This regulatory network was inferred from the input dataset. The miRNAs and mRNAs are
presented as round and rectangle nodes respectively. The numerical value popped up upon mouse over the gene node is the log2 transformed fold-change of the gene expression between the two groups. All of the nodes are clickable, and the detailed information of the miRNAs/mRNAs and related cancer pathway will be displayed in another window. The edges between nodes are supported by both interactions (predicted or experimentally verified) and correlations learnt from cancer dataset. The numerical value popped up upon mouse over the edge is the correlation beat value (effect size) between the two nodes. The experimental evidences of the edges reported in previous cancer studies are highlighted by red/orange color. All of these information can be accessed by the "mouse-over" action. This network shows a full map of the miRNA-mRNA regulation of the input gene list(s), and the hub miRNAs (with the high network degree/betweenness centrality) would be the potential cancer drivers or tumor suppressors. The full result table can be accessed in the "Regulations" tab.
"miRNACancerMAP" is also a network visualization tool for users to draw their regulatory network by personal customization. Users can set the complexity of the network by limiting the number of nodes or edges. And the color of the nodes can be defined by different categories of the mRNAs and miRNAs, such as Gene-Ontology, pathway, and expression status. Users can also select to use network degree or network betweenness centrality to define the node size. And edges can be black or colored by the correlation. Purple edge means negative correlation (mostly found between miRNA and mRNA), and blue edge means positive correlation (found in PPI or miRNA-miRNA sponge effect). We can also add the protein-protein interactions (PPI) into the network. This result will show the cluster of genes regulated by some specific miRNAs. Additionally, miRNA-miRNA edges can be added by the "miRNA sponge" button, presenting some clusters of miRNAs that have the interactions via sponge effect.
| Num | microRNA | Gene | miRNA log2FC | miRNA pvalue | Gene log2FC | Gene pvalue | Interaction | Correlation beta | Correlation P-value | PMID | Reported in cancer studies |
|---|---|---|---|---|---|---|---|---|---|---|---|
| 1 | hsa-let-7b-5p | CBX2 | -0.96 | 0 | 2.25 | 0 | miRNATAP | -0.29 | 0.0003 | NA | |
| 2 | hsa-let-7g-5p | CBX2 | -0.46 | 2.0E-5 | 2.25 | 0 | miRNATAP | -0.48 | 1.0E-5 | NA | |
| 3 | hsa-miR-192-3p | CBX2 | -0.64 | 0.00027 | 2.25 | 0 | mirMAP | -0.36 | 0 | NA | |
| 4 | hsa-miR-29a-3p | CBX2 | -0.86 | 0 | 2.25 | 0 | miRNATAP | -0.31 | 0.00078 | NA | |
| 5 | hsa-miR-29c-3p | CBX2 | -1.44 | 0 | 2.25 | 0 | miRNATAP | -0.49 | 0 | NA | |
| 6 | hsa-miR-3614-5p | CBX2 | -1.66 | 0 | 2.25 | 0 | mirMAP | -0.23 | 5.0E-5 | NA | |
| 7 | hsa-miR-378a-3p | CBX2 | -1.19 | 0 | 2.25 | 0 | mirMAP | -0.26 | 2.0E-5 | NA | |
| 8 | hsa-miR-378c | CBX2 | -1.54 | 0 | 2.25 | 0 | mirMAP | -0.31 | 0 | NA | |
| 9 | hsa-miR-193b-3p | CBX6 | -0.17 | 0.27202 | -0.14 | 0.56236 | mirMAP | -0.38 | 0 | NA | |
| 10 | hsa-miR-194-3p | CBX6 | -0.77 | 3.0E-5 | -0.14 | 0.56236 | mirMAP | -0.26 | 2.0E-5 | NA | |
| 11 | hsa-miR-22-3p | CBX6 | -0.63 | 0 | -0.14 | 0.56236 | MirTarget | -0.47 | 1.0E-5 | NA | |
| 12 | hsa-miR-224-3p | CBX6 | 1.41 | 0 | -0.14 | 0.56236 | mirMAP | -0.16 | 0.00035 | NA | |
| 13 | hsa-miR-28-5p | CBX6 | -0.43 | 0 | -0.14 | 0.56236 | mirMAP | -0.46 | 0.0002 | NA | |
| 14 | hsa-miR-3607-3p | CBX6 | -2.16 | 0 | -0.14 | 0.56236 | mirMAP | -0.13 | 0.00972 | NA | |
| 15 | hsa-miR-378a-5p | CBX6 | -1.59 | 0 | -0.14 | 0.56236 | mirMAP | -0.2 | 0.00061 | NA | |
| 16 | hsa-miR-125a-3p | CECR2 | -0.84 | 4.0E-5 | -0.78 | 0.01282 | miRanda | -0.47 | 0 | NA | |
| 17 | hsa-miR-125a-5p | CECR2 | -0.91 | 0 | -0.78 | 0.01282 | miRanda | -0.52 | 0 | NA | |
| 18 | hsa-miR-200b-3p | CECR2 | -1.29 | 0.00027 | -0.78 | 0.01282 | TargetScan | -0.3 | 0 | NA | |
| 19 | hsa-miR-299-5p | CECR2 | -1.29 | 0 | -0.78 | 0.01282 | miRNATAP | -0.18 | 0.00211 | NA | |
| 20 | hsa-miR-320b | CECR2 | 0.09 | 0.60798 | -0.78 | 0.01282 | miRanda | -0.27 | 0.00158 | NA | |
| 21 | hsa-miR-324-5p | CECR2 | 0.37 | 0.00592 | -0.78 | 0.01282 | miRanda | -0.3 | 0.00744 | NA | |
| 22 | hsa-miR-429 | CECR2 | -1.4 | 7.0E-5 | -0.78 | 0.01282 | PITA; miRanda; miRNATAP | -0.31 | 0 | NA | |
| 23 | hsa-miR-130b-5p | CHD3 | 0.17 | 0.33761 | 0.69 | 0.00024 | mirMAP | -0.26 | 0 | NA | |
| 24 | hsa-miR-23b-5p | CHD3 | -1.05 | 0 | 0.69 | 0.00024 | MirTarget | -0.21 | 0.00083 | NA | |
| 25 | hsa-miR-28-5p | CHD3 | -0.43 | 0 | 0.69 | 0.00024 | miRanda | -0.58 | 0 | NA | |
| 26 | hsa-miR-1269a | EYA2 | 3.58 | 0 | -2.25 | 0 | MirTarget | -0.12 | 1.0E-5 | NA | |
| 27 | hsa-miR-30d-5p | EYA2 | 0.72 | 0 | -2.25 | 0 | miRNATAP | -0.46 | 0.00041 | NA | |
| 28 | hsa-let-7b-5p | EZH2 | -0.96 | 0 | 2.57 | 0 | miRNATAP | -0.27 | 3.0E-5 | 25611389 | Significant inverse correlation between EZH2 and hsa-miR-26a-5p R2=0.56 P=0.0001 and hsa-let-7b-5p R2=0.19 P=0.02 expression was observed in the same samples corroborating the belief of EZH2 being a bona fide target for these two miRNAs in CRC |
| 29 | hsa-let-7g-5p | EZH2 | -0.46 | 2.0E-5 | 2.57 | 0 | miRNATAP | -0.28 | 0.00176 | NA | |
| 30 | hsa-miR-101-3p | EZH2 | -1.48 | 0 | 2.57 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.76 | 0 | 24002871; 26718325; 24211739; 26251675; 22108826; 24490857; 23962556; 21818714; 25260883; 25428391; 27620004; 22450781; 25400732; 25190211; 22977606; 24807198; 21321380; 22094936; 21270667 | miR-101 in turn inhibits the expression of two subunits of PRC2 EZH2 and EED thus creating a double-negative feedback loop that regulates the process of hepatocarcinogenesis; In addition co-overexpression of c-Myc and EZH2 in HCC samples was closely associated with lower expression of miR-101 P < 0.0001 and poorer prognosis of HCC patients P < 0.01;Reporter gene assays revealed that ectopic expression of EZH2 inhibited the transcriptional activities of miR-101-1 promoter; Moreover our results also demonstrated that similar antitumor effects can be achieved either by ectopic miR-101 or EZH2 silencing in HCC cells; These findings show that elevated EZH2 contributes to miR-101 deregulation in HCC and highlight the coordinated role of miR-101 and EZH2 in hepatocarcinogenesis;The aim of our study was to investigate the functional role of both miR-101 and EZH2 in human hepatocellular carcinoma HCC; MiR-101 and EZH2 expressions were evaluated in tumor tissues of 99 HCC patients and 7 liver cancer cell lines by real-time PCR; Luciferase reporter assay was employed to validate whether EZH2 represents a target gene of miR-101; MiR-101 expression was significantly downregulated in most of HCC tissues and all cell lines whereas EZH2 was significantly overexpressed in most of HCC tissues and all cell lines; There was a negative correlation between expression levels of miR-101 and EZH2; Luciferase assay results confirmed EZH2 as a direct target gene of miR-101 which negatively regulates EZH2 expression in HCC; Tumor suppressor miR-101 represses HCC progression through directly targeting EZH2 oncogene and sensitizes liver cancer cells to chemotherapeutic treatment;MiR-101 is a microRNA involved in a negative feedback circuit with EZH2 in different normal and tumor tissues; To that miR-101 can behave as a tumor suppressor in several cancers by repressing EZH2 expression; We therefore evaluated whether miR-101 is de-regulated in eRMS and investigated its interplaying with EZH2 as well as its role in the in vitro tumorigenic potential of these tumor cells; Herein we report that miR-101 is down-regulated in eRMS patients and in tumor cell lines compared to their controls showing an inverse pattern of expression with EZH2; We also show that miR-101 is up-regulated in eRMS cells following both genetic and pharmacological inhibition of EZH2; In turn miR-101 forced expression reduces EZH2 levels as well as restrains the migratory potential of eRMS cells and impairs their clonogenic and anchorage-independent growth capabilities; This phenomenon is associated to reduced H3K27me3 levels at the same regulatory locus indicating that EZH2 directly targets miR-101 for repression in eRMS cells; Altogether our data show that in human eRMS miR-101 is involved in a negative feedback loop with EZH2 whose targeting has been previously shown to halt eRMS tumorigenicity;Mechanistic investigations revealed that reexpression of miR-101 was sufficient to limit the expression of EZH2 and the proinvasive cell surface adhesion molecule EpCAM;Methyl jasmonate sensitizes human bladder cancer cells to gambogic acid induced apoptosis through down regulation of EZH2 expression by miR 101; Furthermore treatment of bladder cancer cells with a combination of GA and MJ induced synergistic inhibition of the enhancer of zeste homologue 2 EZH2 expression whereas miR-101 expression was up-regulated; Conversely knockdown of miR-101 restored this decreased expression of EZH2 and suppressed the inhibitory effect of GA and MJ on the growth of bladder cancer cells; MJ sensitizes bladder cancer cells to GA-induced apoptosis by down-regulating the expression of EZH2 induced by miR-101;MiR 101 inhibits melanoma cell invasion and proliferation by targeting MITF and EZH2; Functional assays showed that miR-101 suppressed invasion and proliferation - an outcome that could be phenocopied by siRNA knockdown of MITF and EZH2;We explore the role of miR-101 and its interaction with EzH2 in epithelial ovarian carcinoma EOC; CHIP assays revealed that re-expression of miR-101 inhibited the interaction of EzH2 with p21waf1/cip1 promoter;miR 101 regulates expression of EZH2 and contributes to progression of and cisplatin resistance in epithelial ovarian cancer; miR-101 overexpression decreased the expression of EZH2 reduced proliferation and migration of ovarian cancer cells and resensitized drug-resistant cancer cells to cisplatin-induced cytotoxicity suggesting the important role miR-101 plays in ovarian cancer that may be associated with its function as a regulator targeting EZH2;The results showed that mir-101 was down-regulated and EZH2 were upregulated; Subsequently the roles of mir-101 and EZH2 in tumor growth and progression in vitro were tested; Overexpression of mir-101 mimics was able to suppress the expression of EZH2 in XWLC-05 cells; Interleukin-1β subsequently induces the downregulation of mir-101 which may result in the upregulated level of EZH2 and occurrence of lung cancer;Long non coding RNA XIST regulates gastric cancer progression by acting as a molecular sponge of miR 101 to modulate EZH2 expression;Moreover around 40% of cases showing miR-101 down-regulation displayed concomitant EZH2 over-expression at the RNA and protein levels which in turn was associated with loss/aberrant expression of E-cadherin; In conclusion we show that deletions and/or microdeletions at both miR-101 genomic loci cause mature miR-101 down-regulation subsequent EZH2 over-expression and E-cadherin dysfunction specifically in intestinal-type GC;miR 101 suppresses tumor proliferation and migration and induces apoptosis by targeting EZH2 in esophageal cancer cells; The expression level of miR-101 was inversely correlated to EZH2 protein expression in ESCC cell; These findings suggest that decreased expression of miR-101 might promote metastasis of human ESCC by inducing accumulation of EZH2 protein;In the present study we reported that ectopic overexpression of miR-101 downregulated the expression level of EZH2 and significantly inhibited migration and invasion of osteosarcoma cells; In addition knockdown of EZH2 by siRNA showed the same effect of miR-101 on migration and invasion; To conclude these results indicate that miR-101 may act as a tumor suppressor in osteosarcoma as it has a suppressive role in cell migration and invasion by targeting EZH2;Therefore we aimed to ascertain whether or not the overexpression of miR-101 inhibits invasion of lung cancer through regulation of EZH2; In this study the expression of miR-101 was down-regulated and the expression of EZH2 was up-regulated in lung cancer; Overexpression of miR-101 induced a marked reduction in EZH2 mRNA levels in several lung cancer cell lines; miR-101 may be a potent tumor suppressor by altering chromatin structure through repression of EZH2 and may be a potential therapeutic tool for patients with lung cancer;MiR 101 downregulated in retinoblastoma functions as a tumor suppressor in human retinoblastoma cells by targeting EZH2; Finally we found that miR-101 directly inhibited EZH2 expression by targeting its 3'-UTR and EZH2 was upregulated and inversely correlated with miR-101 expression in the retinoblastoma tissues; Thus for the first time we provide convincing evidence that downregulation of miR-101 is associated with tumor aggressiveness in retinoblastoma and inhibits cell growth and proliferation of retinoblastoma cells by targeting EZH2;miR 101 is down regulated in glioblastoma resulting in EZH2 induced proliferation migration and angiogenesis; Here we determined that miR-101 is down-regulated in GBM resulting in overexpression of the miR-101 target PcG protein EZH2 a histone methyltransferase affecting gene expression profiles in an epigenetic manner; Our results indicate that EZH2 has a versatile function in GBM progression and that its overexpression is at least partly due to decreased miR-101 expression;Main objective of the present study is to investigate miR-26a and miR-101 levels which both target EZH2 for their association with molecular pathways and with efficacy of tamoxifen as first-line monotherapy for metastatic breast cancer;In this study we investigate whether miRNA miR-101 regulates EZH2 expression in NSCLC; We evaluated the expression of miR-101 and EZH2 in 20 matched NSCLC and adjacent nontumor lung tissues by reverse-transcriptase polymerase chain reaction and immunohistochemistry respectively; Luciferase reporter assay was used to determine whether miR-101 directly targets EZH2; To assess the effect of miR-101 on NSCLC biological behavior cell proliferation invasion and response to chemotherapy were analyzed using NSCLC cells transfected with miR-101 mimics or transfected with specific small interfering RNA to deplete EZH2 small interfering RNA-EZH2; Reduced expression of miR-101 was associated with overexpression of EZH2 in NSCLC tumor tissues; Transfection of miR-101 mimics significantly suppressed the activity of the luciferase reporter containing wild type but not mutant EZH2 3'-UTR and decreased EZH2 expression in NSCLC cell lines; Therapeutic strategies to rescue miR-101 expression or silence EZH2 may be beneficial to patients with NSCLC in the future |
| 31 | hsa-miR-139-5p | EZH2 | -2.11 | 0 | 2.57 | 0 | miRanda | -0.59 | 0 | NA | |
| 32 | hsa-miR-144-3p | EZH2 | -2.98 | 0 | 2.57 | 0 | miRNATAP | -0.26 | 0 | 23815091 | miR 144 downregulation increases bladder cancer cell proliferation by targeting EZH2 and regulating Wnt signaling |
| 33 | hsa-miR-199a-5p | EZH2 | -1.99 | 0 | 2.57 | 0 | miRNAWalker2 validate | -0.2 | 0 | NA | |
| 34 | hsa-miR-26a-5p | EZH2 | -0.96 | 0 | 2.57 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.55 | 0 | 26733151; 25494962; 20952513; 23750239; 25611389; 24452597; 21901171; 27517917; 22086681; 27562865; 22930729; 22094936 | Through down-regulation of EZH2 expression and up-regulation of E-cadherin expression miR-26a inhibited the EMT process in vitro and in vivo; Luciferase reporter assay showed that miR-26a directly interacted with EZH2 messenger RNA mRNA; Furthermore the expression of miR-26a was positively correlated with E-cadherin expression and inversely correlated with EZH2 expression in human HCC tissue; miR-26a inhibited the EMT process in HCC by down-regulating EZH2 expression;miR 26a promoted by interferon alpha inhibits hepatocellular carcinoma proliferation and migration by blocking EZH2; Here we report that the IFN-α-induced microRNA-26a miR-26a can inhibit HCC proliferation and invasion by suppressing enhancer of zeste homologue 2 EZH2 expression in tumor cells; It was shown that there was increased miR-26a accompanied with downregulated EZH2 expression in the HCC specimens and EZH2 mRNA levels were inversely correlated with miR-26a expression; In addition the miR-26a mimic transfection decreased the EZH2 expression level significantly in the transfected HepG2 cells and inhibited HepG2 cell proliferation and invasion effectively; Our results indicate that miR-26a exerts growth inhibition in HCC and that its inhibitory effect is mediated briefly by blocking EZH2 expression;Pathologically decreased miR 26a antagonizes apoptosis and facilitates carcinogenesis by targeting MTDH and EZH2 in breast cancer; Subsequently MTDH and EZH2 are identified as two direct targets of miR-26a and they are significantly upregulated in breast cancer; MCF7 xenografts with exogenous miR-26a show that a decrease in expression of both MTDH and EZH2 is accompanied by an increase in apoptosis; Our findings suggest that miR-26a functionally antagonizes human breast carcinogenesis by targeting MTDH and EZH2;MiR-26a has been reported as a tumor suppressor microRNA in breast cancer which is attributed mainly to targeting of MTDH and EZH2 however the expression profile and therapeutic potential of miR-26a is still unclear;Significant inverse correlation between EZH2 and hsa-miR-26a-5p R2=0.56 P=0.0001 and hsa-let-7b-5p R2=0.19 P=0.02 expression was observed in the same samples corroborating the belief of EZH2 being a bona fide target for these two miRNAs in CRC;Moreover EZH2 was upregulated and inversely correlated with miR-26a expression in the osteosarcoma tissues; Thus for the first time we provide convincing evidence that downregulation of miR-26a is associated with tumor aggressiveness and tumor metastasis and miR-26a inhibits cell migration and invasion by targeting the EZH2 gene in osteosarcoma;Previously EZH2 was shown to be regulated by miR-26a at the translational levels in lymphomas;miR-26a inhibition partly prevents the metformin viability effect and the PTEN and EZH2 expression reduction;We also found that reexpression of miR-26a by transfection led to decreased expression of EZH2 and EpCAM in pancreatic cancer cells;In the present study the influence of miR-26a and miR-138 on EZH2 and cellular function including the impact on the cell cycle regulating network was evaluated in PCa cells; The present findings suggest an anti-proliferative role for miR-26a and miR-138 in PCa by blocking the G1/S-phase transition independent of EZH2 but via a concerted inhibition of crucial cell cycle regulators;We propose the hypermethylation of miR-26a as an alternative pathway of ERG rearrangement-independent EZH2 activation;High miR 26a and low CDC2 levels associate with decreased EZH2 expression and with favorable outcome on tamoxifen in metastatic breast cancer; Main objective of the present study is to investigate miR-26a and miR-101 levels which both target EZH2 for their association with molecular pathways and with efficacy of tamoxifen as first-line monotherapy for metastatic breast cancer; Cell cycle regulation and CCNE1 and CDC2 were the only significant overlapping pathway and genes differentially expressed between tumors with high and low levels of miR-26a and EZH2 respectively; Cell cycle regulation is the only overlapping pathway linked to miR-26a and EZH2 levels; Low mRNA levels of EZH2 CCNE1 and CDC2 and high levels of miR-26a are associated with favorable outcome on tamoxifen |
| 35 | hsa-miR-26b-5p | EZH2 | -1.11 | 0 | 2.57 | 0 | MirTarget; miRNATAP | -0.6 | 0 | NA | |
| 36 | hsa-miR-450b-5p | EZH2 | -1.34 | 0 | 2.57 | 0 | MirTarget; PITA; miRNATAP | -0.37 | 0 | NA | |
| 37 | hsa-miR-193a-5p | HDAC9 | -0.47 | 1.0E-5 | -1.16 | 0 | PITA | -0.36 | 0.00014 | NA | |
| 38 | hsa-miR-30d-5p | HDAC9 | 0.72 | 0 | -1.16 | 0 | miRNATAP | -0.36 | 0 | NA | |
| 39 | hsa-miR-361-5p | HDAC9 | 0.23 | 0.00962 | -1.16 | 0 | PITA; miRanda; miRNATAP | -0.38 | 0.00097 | NA | |
| 40 | hsa-miR-455-5p | HDAC9 | -0.27 | 0.05813 | -1.16 | 0 | miRanda | -0.42 | 0 | NA | |
| 41 | hsa-miR-618 | HDAC9 | 0.14 | 0.51715 | -1.16 | 0 | PITA | -0.27 | 0 | NA | |
| 42 | hsa-let-7b-3p | HELLS | -1.22 | 0 | 2.62 | 0 | mirMAP | -0.69 | 0 | NA | |
| 43 | hsa-let-7b-5p | HELLS | -0.96 | 0 | 2.62 | 0 | miRNAWalker2 validate | -0.35 | 2.0E-5 | NA | |
| 44 | hsa-let-7f-1-3p | HELLS | -0.7 | 0 | 2.62 | 0 | mirMAP | -0.37 | 2.0E-5 | NA | |
| 45 | hsa-miR-148a-5p | HELLS | -0.77 | 0 | 2.62 | 0 | mirMAP | -0.21 | 0.00818 | NA | |
| 46 | hsa-miR-193b-3p | HELLS | -0.17 | 0.27202 | 2.62 | 0 | miRNAWalker2 validate | -0.22 | 0.00631 | NA | |
| 47 | hsa-miR-195-3p | HELLS | -1.09 | 0 | 2.62 | 0 | mirMAP | -0.25 | 0.00012 | NA | |
| 48 | hsa-miR-199a-5p | HELLS | -1.99 | 0 | 2.62 | 0 | miRanda | -0.21 | 0 | NA | |
| 49 | hsa-miR-24-1-5p | HELLS | -1.32 | 0 | 2.62 | 0 | MirTarget | -0.77 | 0 | NA | |
| 50 | hsa-miR-29b-1-5p | HELLS | -0.54 | 0.00103 | 2.62 | 0 | mirMAP | -0.34 | 1.0E-5 | NA | |
| 51 | hsa-miR-30a-3p | HELLS | -1.53 | 0 | 2.62 | 0 | mirMAP | -0.54 | 0 | NA | |
| 52 | hsa-miR-30e-3p | HELLS | -1.21 | 0 | 2.62 | 0 | mirMAP | -0.53 | 0 | NA | |
| 53 | hsa-miR-3607-3p | HELLS | -2.16 | 0 | 2.62 | 0 | mirMAP | -0.35 | 0 | NA | |
| 54 | hsa-miR-374b-5p | HELLS | -0.31 | 0.00301 | 2.62 | 0 | MirTarget; mirMAP | -0.32 | 0.00689 | NA | |
| 55 | hsa-miR-450b-5p | HELLS | -1.34 | 0 | 2.62 | 0 | mirMAP | -0.32 | 1.0E-5 | NA | |
| 56 | hsa-miR-107 | IKZF1 | 0.24 | 0.01708 | -0.97 | 0 | miRanda | -0.33 | 0.00048 | NA | |
| 57 | hsa-miR-219a-1-3p | IKZF1 | -0.07 | 0.64586 | -0.97 | 0 | MirTarget | -0.3 | 1.0E-5 | NA | |
| 58 | hsa-miR-32-3p | IKZF1 | 0.22 | 0.20722 | -0.97 | 0 | mirMAP | -0.15 | 0.00706 | NA | |
| 59 | hsa-miR-32-5p | IKZF1 | 0.08 | 0.54898 | -0.97 | 0 | miRNATAP | -0.23 | 0.00118 | NA | |
| 60 | hsa-miR-33a-3p | IKZF1 | -0.68 | 1.0E-5 | -0.97 | 0 | mirMAP | -0.17 | 0.00645 | NA | |
| 61 | hsa-miR-361-5p | IKZF1 | 0.23 | 0.00962 | -0.97 | 0 | miRanda | -0.45 | 3.0E-5 | NA | |
| 62 | hsa-miR-616-5p | IKZF1 | 0.15 | 0.40284 | -0.97 | 0 | mirMAP | -0.22 | 4.0E-5 | NA | |
| 63 | hsa-miR-93-3p | IKZF1 | 0.4 | 0.00131 | -0.97 | 0 | mirMAP | -0.22 | 0.00379 | NA | |
| 64 | hsa-miR-106a-5p | KAT2B | -0.46 | 0.00972 | -0.94 | 0 | MirTarget | -0.18 | 1.0E-5 | NA | |
| 65 | hsa-miR-106b-5p | KAT2B | 0.65 | 0 | -0.94 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget | -0.52 | 0 | NA | |
| 66 | hsa-miR-125a-3p | KAT2B | -0.84 | 4.0E-5 | -0.94 | 0 | miRanda | -0.15 | 4.0E-5 | NA | |
| 67 | hsa-miR-17-5p | KAT2B | 0.7 | 2.0E-5 | -0.94 | 0 | MirTarget; TargetScan | -0.4 | 0 | 23095762 | miR 17 5p targets the p300/CBP associated factor and modulates androgen receptor transcriptional activity in cultured prostate cancer cells; Targeting of PCAF by miR-17-5p was evaluated using the luciferase reporter assay; Expression of PCAF in PCa cells was associated with the downregulation of miR-17-5p; Targeting of the 3'-untranslated region of PCAF mRNA by miR-17-5p caused translational suppression and RNA degradation and consequently modulation of AR transcriptional activity in PCa cells; PCAF is upregulated in cultured PCa cells and upregulation of PCAF is associated with the downregulation of miR-17-5p; Targeting of PCAF by miR-17-5p modulates AR transcriptional activity and cell growth in cultured PCa cells |
| 68 | hsa-miR-181a-5p | KAT2B | 0.25 | 0.05519 | -0.94 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget | -0.43 | 0 | NA | |
| 69 | hsa-miR-181b-5p | KAT2B | 0.49 | 0.00105 | -0.94 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget | -0.46 | 0 | NA | |
| 70 | hsa-miR-181c-5p | KAT2B | -0.01 | 0.96913 | -0.94 | 0 | MirTarget | -0.27 | 0 | NA | |
| 71 | hsa-miR-181d-5p | KAT2B | 0.16 | 0.36381 | -0.94 | 0 | MirTarget | -0.28 | 0 | NA | |
| 72 | hsa-miR-19a-3p | KAT2B | 1.02 | 0 | -0.94 | 0 | miRNAWalker2 validate | -0.26 | 0 | NA | |
| 73 | hsa-miR-19b-3p | KAT2B | 0.6 | 0.00017 | -0.94 | 0 | miRNAWalker2 validate | -0.3 | 0 | NA | |
| 74 | hsa-miR-20a-3p | KAT2B | -0.32 | 0.04679 | -0.94 | 0 | MirTarget | -0.22 | 0 | NA | |
| 75 | hsa-miR-20a-5p | KAT2B | 0.85 | 0 | -0.94 | 0 | MirTarget | -0.32 | 0 | NA | |
| 76 | hsa-miR-20b-5p | KAT2B | 0.46 | 0.02859 | -0.94 | 0 | MirTarget | -0.11 | 0.00122 | NA | |
| 77 | hsa-miR-25-3p | KAT2B | 0.63 | 0 | -0.94 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget | -0.26 | 0.00023 | NA | |
| 78 | hsa-miR-330-3p | KAT2B | -0.33 | 0.03161 | -0.94 | 0 | MirTarget | -0.27 | 0 | NA | |
| 79 | hsa-miR-338-5p | KAT2B | -0.22 | 0.25239 | -0.94 | 0 | MirTarget; miRNATAP | -0.15 | 7.0E-5 | NA | |
| 80 | hsa-miR-342-3p | KAT2B | -0.32 | 0.04498 | -0.94 | 0 | miRanda | -0.18 | 7.0E-5 | NA | |
| 81 | hsa-miR-363-3p | KAT2B | -0.17 | 0.37519 | -0.94 | 0 | MirTarget | -0.1 | 0.00633 | NA | |
| 82 | hsa-miR-429 | KAT2B | -1.4 | 7.0E-5 | -0.94 | 0 | miRanda | -0.13 | 0 | NA | |
| 83 | hsa-miR-590-5p | KAT2B | -0.1 | 0.31003 | -0.94 | 0 | miRanda | -0.26 | 0.0004 | NA | |
| 84 | hsa-miR-92a-3p | KAT2B | 0.21 | 0.13429 | -0.94 | 0 | miRNAWalker2 validate; MirTarget | -0.35 | 0 | NA | |
| 85 | hsa-miR-92b-3p | KAT2B | 0.22 | 0.29619 | -0.94 | 0 | MirTarget | -0.23 | 0 | NA | |
| 86 | hsa-miR-93-5p | KAT2B | 1.4 | 0 | -0.94 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget | -0.38 | 0 | NA | |
| 87 | hsa-miR-26b-5p | KDM5D | -1.11 | 0 | 0.9 | 0.20909 | miRNAWalker2 validate | -0.86 | 0.00297 | NA | |
| 88 | hsa-miR-335-5p | KDM5D | -1.61 | 0 | 0.9 | 0.20909 | miRNAWalker2 validate | -0.51 | 0.00656 | NA | |
| 89 | hsa-miR-101-3p | LMNB1 | -1.48 | 0 | 0.98 | 0 | miRNAWalker2 validate; MirTarget; miRNATAP | -0.36 | 0 | NA | |
| 90 | hsa-miR-199a-5p | LMNB1 | -1.99 | 0 | 0.98 | 0 | miRanda | -0.11 | 0.00013 | NA | |
| 91 | hsa-miR-26b-5p | LMNB1 | -1.11 | 0 | 0.98 | 0 | miRNAWalker2 validate | -0.21 | 0.00338 | NA | |
| 92 | hsa-miR-3065-3p | LMNB1 | -1.04 | 5.0E-5 | 0.98 | 0 | MirTarget; miRNATAP | -0.12 | 0.00052 | NA | |
| 93 | hsa-miR-30a-3p | LMNB1 | -1.53 | 0 | 0.98 | 0 | miRNATAP | -0.29 | 0 | NA | |
| 94 | hsa-miR-122-5p | LMNB2 | -1.24 | 0 | 1.16 | 0 | miRNAWalker2 validate | -0.28 | 0 | NA | |
| 95 | hsa-miR-125b-5p | LMNB2 | -1.36 | 0 | 1.16 | 0 | mirMAP | -0.35 | 0 | NA | |
| 96 | hsa-miR-145-3p | LMNB2 | -1.14 | 0 | 1.16 | 0 | mirMAP | -0.1 | 0.0055 | NA | |
| 97 | hsa-miR-192-5p | LMNB2 | -0.5 | 0.00345 | 1.16 | 0 | miRNAWalker2 validate | -0.29 | 0 | NA | |
| 98 | hsa-miR-193b-3p | LMNB2 | -0.17 | 0.27202 | 1.16 | 0 | miRNAWalker2 validate | -0.27 | 0 | NA | |
| 99 | hsa-miR-195-5p | LMNB2 | -1.86 | 0 | 1.16 | 0 | mirMAP | -0.18 | 0 | NA | |
| 100 | hsa-miR-215-5p | LMNB2 | -0.98 | 3.0E-5 | 1.16 | 0 | miRNAWalker2 validate | -0.14 | 0 | NA | |
| 101 | hsa-miR-30a-5p | LMNB2 | -0.63 | 0.00011 | 1.16 | 0 | miRNAWalker2 validate | -0.13 | 0.00082 | NA | |
| 102 | hsa-miR-424-5p | LMNB2 | -2.63 | 0 | 1.16 | 0 | mirMAP | -0.14 | 1.0E-5 | NA | |
| 103 | hsa-miR-497-5p | LMNB2 | -1.41 | 0 | 1.16 | 0 | mirMAP | -0.18 | 0 | NA | |
| 104 | hsa-miR-664a-5p | LMNB2 | -0.07 | 0.59768 | 1.16 | 0 | mirMAP | -0.21 | 1.0E-5 | NA | |
| 105 | hsa-miR-330-3p | NCOA2 | -0.33 | 0.03161 | -0.55 | 0.06353 | PITA | -0.31 | 0.00141 | NA | |
| 106 | hsa-miR-339-5p | NCOA2 | 0.28 | 0.03557 | -0.55 | 0.06353 | miRanda | -0.49 | 1.0E-5 | NA | |
| 107 | hsa-miR-186-5p | PHC1 | -0.06 | 0.53529 | -0.35 | 0.02268 | mirMAP | -0.2 | 0.00897 | NA | |
| 108 | hsa-miR-22-3p | PHC1 | -0.63 | 0 | -0.35 | 0.02268 | MirTarget | -0.19 | 0.00881 | NA | |
| 109 | hsa-miR-192-5p | PHF19 | -0.5 | 0.00345 | 1.32 | 0 | miRNAWalker2 validate | -0.22 | 0 | NA | |
| 110 | hsa-miR-193b-3p | PHF19 | -0.17 | 0.27202 | 1.32 | 0 | miRNAWalker2 validate | -0.18 | 0.00025 | NA | |
| 111 | hsa-miR-195-5p | PHF19 | -1.86 | 0 | 1.32 | 0 | miRNATAP | -0.14 | 0.00026 | 25955388 | MicroRNA 195 5p acts as an anti oncogene by targeting PHF19 in hepatocellular carcinoma; In addition it has been shown that miR-195 plays an important role in the molecular etiology of HCC; however the effect and possible mechanism of PHF19 on HCC is unclear and the association between PHF19 and miR-195 has seldom been addressed; Our results showed that PHF19 is a potential target of hsa-miR-195-5p based on a bioinformatic analysis and results of a luciferase reporter assay; PHF19 was downregulated after transfection with hsa-miR-195-5p mimics; In contrast overexpression of hsa-miR-195-5p in hepatoma cells reduced PHF19 expression leading to suppression of hepatoma cell invasion migration and proliferation in vitro; In addition PHF19 markedly promoted the growth of xenograft tumors while hsa-miR-195-5p markedly suppressed the growth of xenograft tumors in nude mice; These results provide evidence that PHF19 promotes HCC and is regulated by the tumor-suppressor miR-195-5p |
| 112 | hsa-miR-23b-3p | PHF19 | -0.53 | 0 | 1.32 | 0 | miRNATAP | -0.28 | 8.0E-5 | NA | |
| 113 | hsa-miR-3614-5p | PHF19 | -1.66 | 0 | 1.32 | 0 | mirMAP | -0.16 | 1.0E-5 | NA | |
| 114 | hsa-miR-424-5p | PHF19 | -2.63 | 0 | 1.32 | 0 | miRNATAP | -0.16 | 3.0E-5 | NA | |
| 115 | hsa-miR-664a-5p | PHF19 | -0.07 | 0.59768 | 1.32 | 0 | mirMAP | -0.36 | 0 | NA | |
| 116 | hsa-miR-125b-2-3p | PRDM16 | -1.66 | 0 | -0.04 | 0.92052 | MirTarget | -0.43 | 0 | NA | |
| 117 | hsa-miR-1269a | PRDM16 | 3.58 | 0 | -0.04 | 0.92052 | mirMAP | -0.14 | 0 | NA | |
| 118 | hsa-miR-130b-3p | PRDM16 | 0.69 | 0.00011 | -0.04 | 0.92052 | mirMAP | -0.35 | 0.00023 | NA | |
| 119 | hsa-miR-144-3p | PRDM16 | -2.98 | 0 | -0.04 | 0.92052 | MirTarget; miRNATAP | -0.22 | 0.00014 | NA | |
| 120 | hsa-miR-186-5p | PRDM16 | -0.06 | 0.53529 | -0.04 | 0.92052 | mirMAP | -0.63 | 0.00041 | NA | |
| 121 | hsa-miR-193b-3p | PRDM16 | -0.17 | 0.27202 | -0.04 | 0.92052 | mirMAP | -0.68 | 0 | NA | |
| 122 | hsa-miR-219a-5p | PRDM16 | 0.18 | 0.32269 | -0.04 | 0.92052 | MirTarget | -0.32 | 0.00119 | NA | |
| 123 | hsa-miR-30c-1-3p | PRDM16 | -1.39 | 0 | -0.04 | 0.92052 | mirMAP | -0.47 | 0 | NA | |
| 124 | hsa-miR-30e-3p | PRDM16 | -1.21 | 0 | -0.04 | 0.92052 | mirMAP | -0.41 | 0.00286 | NA | |
| 125 | hsa-miR-378a-3p | PRDM16 | -1.19 | 0 | -0.04 | 0.92052 | mirMAP | -0.46 | 0 | NA | |
| 126 | hsa-miR-378c | PRDM16 | -1.54 | 0 | -0.04 | 0.92052 | mirMAP | -0.39 | 0 | NA | |
| 127 | hsa-miR-548b-3p | PRDM16 | -0.02 | 0.93082 | -0.04 | 0.92052 | mirMAP | -0.51 | 0 | NA | |
| 128 | hsa-miR-550a-3p | PRDM16 | 0.04 | 0.79897 | -0.04 | 0.92052 | miRNATAP | -0.33 | 0.00163 | NA | |
| 129 | hsa-miR-618 | PRDM16 | 0.14 | 0.51715 | -0.04 | 0.92052 | mirMAP | -0.34 | 4.0E-5 | NA | |
| 130 | hsa-miR-146b-3p | RAD54L | -1.21 | 0 | 3.38 | 0 | miRNATAP | -0.2 | 0.00462 | NA | |
| 131 | hsa-miR-26b-5p | RAD54L | -1.11 | 0 | 3.38 | 0 | miRNAWalker2 validate | -0.81 | 0 | NA | |
| 132 | hsa-miR-126-5p | TET1 | -0.43 | 7.0E-5 | 1.02 | 1.0E-5 | mirMAP | -0.41 | 7.0E-5 | NA | |
| 133 | hsa-miR-29a-3p | TET1 | -0.86 | 0 | 1.02 | 1.0E-5 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.97 | 0 | 25367851; 25616722; 27555295 | Negative feedback of miR 29 family TET1 involves in hepatocellular cancer; MiR-29b was proved to inhibit metastasis through the targeting of TET1 indicating that downregulation of miR-29 may involve in HCC carcinogenesis and progression through potentiation of TET1 expression;Erratum to: Negative feedback of miR 29 family TET1 involves in hepatocellular cancer; miR-29b was proved to inhibit metastasis through the targeting of TET1 indicating that downregulation of miR-29 may involve in HCC carcinogenesis and progression through potentiation of TET1 expression;Furthermore data from bioinformatic analysis validated by dual-luciferase reporter gene assay showed that ten eleven translocation 1 TET1 was a direct target of miR-29a and over-expression of TET1 inhibited cell proliferation and migration which could be induced by the up-regulation of miR-29a; MiR-29a targets TET1 down regulates its expression and thus promotes EMT in breast cancer; Altogether we demonstrate that miR-29a acts as a tumor activator by targeting TET1 and induces cell proliferation and EMT in breast cancer |
| 134 | hsa-miR-29b-3p | TET1 | -0.35 | 0.01214 | 1.02 | 1.0E-5 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.71 | 0 | 25367851; 25616722 | Negative feedback of miR 29 family TET1 involves in hepatocellular cancer; MiR-29b was proved to inhibit metastasis through the targeting of TET1 indicating that downregulation of miR-29 may involve in HCC carcinogenesis and progression through potentiation of TET1 expression;Erratum to: Negative feedback of miR 29 family TET1 involves in hepatocellular cancer; miR-29b was proved to inhibit metastasis through the targeting of TET1 indicating that downregulation of miR-29 may involve in HCC carcinogenesis and progression through potentiation of TET1 expression |
| 135 | hsa-miR-29c-3p | TET1 | -1.44 | 0 | 1.02 | 1.0E-5 | MirTarget; miRNATAP | -0.76 | 0 | NA | |
| 136 | hsa-miR-30a-3p | TET1 | -1.53 | 0 | 1.02 | 1.0E-5 | MirTarget | -0.24 | 4.0E-5 | NA | |
| 137 | hsa-miR-30d-3p | TET1 | -0.12 | 0.32955 | 1.02 | 1.0E-5 | MirTarget | -0.31 | 0.00061 | NA | |
| 138 | hsa-let-7b-5p | UHRF1 | -0.96 | 0 | 3.5 | 0 | miRNAWalker2 validate | -0.29 | 0.00248 | NA | |
| 139 | hsa-miR-10a-5p | UHRF1 | -1.48 | 0 | 3.5 | 0 | miRNAWalker2 validate | -0.4 | 0 | NA | |
| 140 | hsa-miR-139-5p | UHRF1 | -2.11 | 0 | 3.5 | 0 | miRanda | -0.87 | 0 | NA | |
| 141 | hsa-miR-378a-3p | UHRF1 | -1.19 | 0 | 3.5 | 0 | MirTarget | -0.38 | 0 | NA | |
| 142 | hsa-miR-378c | UHRF1 | -1.54 | 0 | 3.5 | 0 | MirTarget | -0.49 | 0 | NA | |
| 143 | hsa-miR-320b | UTY | 0.09 | 0.60798 | 0.51 | 0.43067 | PITA; miRanda | -0.47 | 0.00867 | NA |
| Num | GO | Overlap | Size | P Value | Adj. P Value |
|---|---|---|---|---|---|
| 1 | CHROMATIN MODIFICATION | 18 | 539 | 5.248e-26 | 2.442e-22 |
| 2 | CHROMATIN ORGANIZATION | 18 | 663 | 2.261e-24 | 5.26e-21 |
| 3 | CHROMOSOME ORGANIZATION | 19 | 1009 | 3.667e-23 | 5.688e-20 |
| 4 | COVALENT CHROMATIN MODIFICATION | 12 | 345 | 1.467e-16 | 1.707e-13 |
| 5 | PEPTIDYL LYSINE MODIFICATION | 7 | 312 | 2.027e-08 | 1.886e-05 |
| 6 | NEGATIVE REGULATION OF TRANSCRIPTION FROM RNA POLYMERASE II PROMOTER | 8 | 740 | 4.486e-07 | 0.0002982 |
| 7 | REGULATION OF TRANSCRIPTION FROM RNA POLYMERASE II PROMOTER | 11 | 1784 | 4.187e-07 | 0.0002982 |
| 8 | NEGATIVE REGULATION OF GENE EXPRESSION | 10 | 1493 | 8.571e-07 | 0.0004985 |
| 9 | REGULATION OF GENE EXPRESSION EPIGENETIC | 5 | 229 | 3.301e-06 | 0.001707 |
| 10 | DNA METABOLIC PROCESS | 7 | 758 | 7.977e-06 | 0.003712 |
| 11 | NEGATIVE REGULATION OF NITROGEN COMPOUND METABOLIC PROCESS | 9 | 1517 | 1.031e-05 | 0.004363 |
| 12 | PEPTIDYL AMINO ACID MODIFICATION | 7 | 841 | 1.571e-05 | 0.006092 |
| 13 | REGULATION OF CHROMATIN ORGANIZATION | 4 | 152 | 1.735e-05 | 0.006211 |
| 14 | DEMETHYLATION | 3 | 54 | 2.391e-05 | 0.007946 |
| Num | GO | Overlap | Size | P Value | Adj. P Value |
|---|
| Num | GO | Overlap | Size | P Value | Adj. P Value |
|---|---|---|---|---|---|
| 1 | PCG PROTEIN COMPLEX | 5 | 43 | 7.165e-10 | 4.184e-07 |
| 2 | HETEROCHROMATIN | 4 | 67 | 6.594e-07 | 0.0001926 |
| 3 | CHROMATIN | 6 | 441 | 4.551e-06 | 0.000886 |
| 4 | TRANSFERASE COMPLEX | 6 | 703 | 6.373e-05 | 0.005745 |
| 5 | HISTONE METHYLTRANSFERASE COMPLEX | 3 | 71 | 5.446e-05 | 0.005745 |
| 6 | PRC1 COMPLEX | 2 | 12 | 6.887e-05 | 0.005745 |
| 7 | CATALYTIC COMPLEX | 7 | 1038 | 6.081e-05 | 0.005745 |
| 8 | METHYLTRANSFERASE COMPLEX | 3 | 90 | 0.0001105 | 0.008068 |
| 9 | ESC E Z COMPLEX | 2 | 16 | 0.0001249 | 0.008104 |
| Num | Pathway | Pathview | Overlap | Size | P Value | Adj. P Value |
|---|
| Num | lncRNA | miRNAs | miRNAs count | Gene | Sponge regulatory network | lncRNA log2FC | lncRNA pvalue | Gene log2FC | Gene pvalue | lncRNA-gene Pearson correlation |
|---|---|---|---|---|---|---|---|---|---|---|
| 1 | SNHG1 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p;hsa-miR-450b-5p | 11 | HELLS | Sponge network | 2.013 | 0 | 2.623 | 0 | 0.703 |
| 2 | RP5-1074L1.4 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-195-3p;hsa-miR-199a-5p;hsa-miR-24-1-5p;hsa-miR-29b-1-5p;hsa-miR-30a-3p;hsa-miR-3607-3p;hsa-miR-450b-5p | 11 | HELLS | Sponge network | 2.302 | 0 | 2.623 | 0 | 0.638 |
| 3 | MAFG-AS1 | hsa-miR-122-5p;hsa-miR-125b-5p;hsa-miR-145-3p;hsa-miR-192-5p;hsa-miR-193b-3p;hsa-miR-195-5p;hsa-miR-215-5p;hsa-miR-424-5p;hsa-miR-497-5p;hsa-miR-664a-5p | 10 | LMNB2 | Sponge network | 2.966 | 0 | 1.155 | 0 | 0.603 |
| 4 | RP11-196G18.22 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-195-3p;hsa-miR-199a-5p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p | 10 | HELLS | Sponge network | 2.705 | 0 | 2.623 | 0 | 0.597 |
| 5 | AP001469.9 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-199a-5p;hsa-miR-29b-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p | 11 | HELLS | Sponge network | 2.428 | 0 | 2.623 | 0 | 0.592 |
| 6 | RP1-228H13.5 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p | 10 | HELLS | Sponge network | 1.554 | 0 | 2.623 | 0 | 0.591 |
| 7 | KB-1572G7.2 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p;hsa-miR-374b-5p | 10 | HELLS | Sponge network | 2.124 | 0 | 2.623 | 0 | 0.584 |
| 8 | TPRG1-AS1 | hsa-miR-106a-5p;hsa-miR-106b-5p;hsa-miR-125a-3p;hsa-miR-17-5p;hsa-miR-181a-5p;hsa-miR-181b-5p;hsa-miR-181c-5p;hsa-miR-181d-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-92a-3p;hsa-miR-92b-3p;hsa-miR-93-5p | 14 | KAT2B | Sponge network | -0.756 | 0.03021 | -0.939 | 0 | 0.573 |
| 9 | RP11-1246C19.1 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-199a-5p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-450b-5p | 10 | HELLS | Sponge network | 2.721 | 0 | 2.623 | 0 | 0.564 |
| 10 | GUSBP11 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-24-1-5p;hsa-miR-29b-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p;hsa-miR-374b-5p | 12 | HELLS | Sponge network | 2.066 | 0 | 2.623 | 0 | 0.541 |
| 11 | RP11-12A2.3 | hsa-miR-106b-5p;hsa-miR-17-5p;hsa-miR-181a-5p;hsa-miR-181b-5p;hsa-miR-181c-5p;hsa-miR-181d-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-25-3p;hsa-miR-92a-3p;hsa-miR-92b-3p;hsa-miR-93-5p | 13 | KAT2B | Sponge network | -4.779 | 0 | -0.939 | 0 | 0.539 |
| 12 | NPSR1-AS1 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-195-3p;hsa-miR-199a-5p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p;hsa-miR-450b-5p | 11 | HELLS | Sponge network | 5.28 | 0 | 2.623 | 0 | 0.53 |
| 13 | CTC-459F4.3 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p | 10 | HELLS | Sponge network | 1.207 | 0 | 2.623 | 0 | 0.51 |
| 14 | RP5-1120P11.1 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-199a-5p;hsa-miR-24-1-5p;hsa-miR-29b-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p | 11 | HELLS | Sponge network | 3.942 | 0 | 2.623 | 0 | 0.51 |
| 15 | TMCC1-AS1 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-195-3p;hsa-miR-199a-5p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-3607-3p;hsa-miR-450b-5p | 10 | HELLS | Sponge network | 2.298 | 0 | 2.623 | 0 | 0.51 |
| 16 | HCG18 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p;hsa-miR-450b-5p | 11 | HELLS | Sponge network | 1.42 | 0 | 2.623 | 0 | 0.5 |
| 17 | AC004862.6 | hsa-miR-106b-5p;hsa-miR-125a-3p;hsa-miR-17-5p;hsa-miR-181a-5p;hsa-miR-181b-5p;hsa-miR-181c-5p;hsa-miR-181d-5p;hsa-miR-19a-3p;hsa-miR-20a-5p;hsa-miR-20b-5p;hsa-miR-93-5p | 11 | KAT2B | Sponge network | -2.202 | 0.00081 | -0.939 | 0 | 0.489 |
| 18 | LINC00238 | hsa-miR-106a-5p;hsa-miR-106b-5p;hsa-miR-125a-3p;hsa-miR-17-5p;hsa-miR-181a-5p;hsa-miR-181b-5p;hsa-miR-181c-5p;hsa-miR-181d-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-20b-5p;hsa-miR-342-3p | 13 | KAT2B | Sponge network | -4.997 | 0 | -0.939 | 0 | 0.478 |
| 19 | LINC00152 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p;hsa-miR-450b-5p | 10 | HELLS | Sponge network | 2.553 | 0 | 2.623 | 0 | 0.451 |
| 20 | MIR4435-1HG | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-195-3p;hsa-miR-24-1-5p;hsa-miR-30a-3p;hsa-miR-30e-3p;hsa-miR-3607-3p;hsa-miR-450b-5p | 10 | HELLS | Sponge network | 2.541 | 0 | 2.623 | 0 | 0.441 |
| 21 | RP11-727A23.5 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-195-3p;hsa-miR-199a-5p;hsa-miR-24-1-5p;hsa-miR-29b-1-5p;hsa-miR-30a-3p;hsa-miR-3607-3p;hsa-miR-450b-5p | 10 | HELLS | Sponge network | 1.435 | 0 | 2.623 | 0 | 0.44 |
| 22 | AC005550.3 | hsa-miR-17-5p;hsa-miR-181a-5p;hsa-miR-181b-5p;hsa-miR-181c-5p;hsa-miR-181d-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-3p;hsa-miR-20a-5p;hsa-miR-92a-3p;hsa-miR-92b-3p | 11 | KAT2B | Sponge network | -2.571 | 0.00132 | -0.939 | 0 | 0.44 |
| 23 | RP11-540A21.2 | hsa-let-7b-3p;hsa-let-7b-5p;hsa-let-7f-1-3p;hsa-miR-148a-5p;hsa-miR-193b-3p;hsa-miR-195-3p;hsa-miR-199a-5p;hsa-miR-24-1-5p;hsa-miR-3607-3p;hsa-miR-450b-5p | 10 | HELLS | Sponge network | 1.758 | 0 | 2.623 | 0 | 0.413 |
| 24 | RP11-747H7.3 | hsa-miR-125b-2-3p;hsa-miR-1269a;hsa-miR-144-3p;hsa-miR-193b-3p;hsa-miR-219a-5p;hsa-miR-30c-1-3p;hsa-miR-378a-3p;hsa-miR-378c;hsa-miR-548b-3p;hsa-miR-618 | 10 | PRDM16 | Sponge network | 0.351 | 0.40524 | -0.035 | 0.92052 | 0.347 |
| 25 | RP11-166D19.1 | hsa-miR-106a-5p;hsa-miR-106b-5p;hsa-miR-17-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-3p;hsa-miR-20a-5p;hsa-miR-25-3p;hsa-miR-590-5p;hsa-miR-92a-3p | 10 | KAT2B | Sponge network | -0.244 | 0.28835 | -0.939 | 0 | 0.254 |