miRNA	gene	miRNA_log2FC	miRNA_pvalue	gene_log2FC	gene_pvalue	interactions	correlation_beta	correlation_pvalue	PMID	evidence	outcome	cancer
hsa-let-7a-5p	HMGA2	-0.439381775414001	3.1119785480023e-05	4.45669314139083	6.73354275393639e-30	miRNAWalker2_validate;miRTarBase;MirTarget;TargetScan	-0.767279337434585	7.45015347476901e-06	20949044;18413822;23073586;21598109;24612219;23134218;23700794;21412931	Since let-7 miRNAs generally play a tumor-suppressive role as targeting oncogenes such as RAS and HMGA2 our results suggest that AZ-P7a cells release let-7 miRNAs via exosomes into the extracellular environment to maintain their oncogenesis;Recent studies report that HMGA2 is negatively regulated by the let-7 microRNA miRNA family; However no studies have examined the clinical significance of HMGA2 and its relationship to the let-7 miRNA family in gastric cancer; We also did an association study comparing HMGA2 expression and let-7 miRNA family expression in gastric cancer; An inverse correlation between HMGA2 and let-7a was found in gastric cancer cell lines P = 0.08; Furthermore our findings suggest that HMGA2 is negatively regulated by the let-7 miRNA family in human gastric cancer;HMGA2 mRNA and let-7 family microRNA were detected by real time fluorescent quantitative reverse transcription polymerase chain reaction in the corresponding frozen tissues; All let-7 family members were detectable in all ovarian cancer samples and their expression were inversely correlated with HMGA2 mRNA expression r=-0.305P<0.05; The downregulation of let-7 is but not the only mechanism of HMGA2 overexpression in serous ovarian cancer;Role of microRNA let 7 and effect to HMGA2 in esophageal squamous cell carcinoma; To investigated the role of microRNA miRNA let-7 and its regulation on high mobility group A2 HMGA2 protein expression in esophageal squamous cell carcinoma ESCC; To evaluate the role of let-7 and HMGA2 cell proliferations were analyzed with synthetic let-7 mimics- or its inhibitor-transfected cells; The transcription of let-7 inversely correlated with HMGA2 protein; The present results demonstrated that let-7 and HMGA2 involved in ESCC carcinogenesis;HMGA2 is down regulated by microRNA let 7 and associated with epithelial mesenchymal transition in oesophageal squamous cell carcinomas of Kazakhs; To investigate the expression of let-7 and its regulation of high-mobility group A2 protein HMGA2 and to verify the relationship between let-7 HMGA2 and the process of epithelial-mesenchymal transition EMT in oesophageal squamous cell carcinomas OSCC of Kazakh patients; Let-7 could repress expression of HMGA2 after co-transfection with let-7 and HMGA2 P = 0.002; Moreover let-7 expression was observed less frequently P = 2.0 × 10-8  and HMGA2 expression more frequently P = 1.0 × 10-10  in OSCC than in normal adjacent tissues; and let-7 expression was observed less frequently in OSCC from Kazakh patients than in those from Han and Uygur patients P = 0.041; There was a reverse correlation between expression of let-7 and HMGA2 P = 0.018; Expression of let-7 can suppress cell proliferation by acting directly on regulation of HMGA2 in OSCC;MicroRNA let 7a inhibits the proliferation and invasion of nonsmall cell lung cancer cell line 95D by regulating K Ras and HMGA2 gene expression; K-RAS and HMGA2 mRNA levels were significantly higher in the let-7a overexpressed group than those in the let-7a inhibited group p < 0.05; However the protein levels of K-RAS and HMGA2 were significantly lower in the let-7a overexpressed group than those in the let-7a inhibited group p < 0.05; We suppose that let-7a inhibits the proliferation and invasion of the cell line 95D by regulating the translation of K-RAS and HMGA2 mRNA not the transcription of the mRNA itself;MiR-98 a member in the let-7 family acts as a negative regulator in the expression of HMGA2 high mobility group A2 oncogene and it has been shown to have a nearly 3-fold decrease in A549/DDP cells;Let 7 microRNA and HMGA2 levels of expression are not inversely linked in adipocytic tumors: analysis of 56 lipomas and liposarcomas with molecular cytogenetic data; The aim of our study was first to assess the role of HMGA2 expression in the pathogenesis of adipocytic tumors AT and second to seek a potential correlation between overexpression of HMGA2 and let-7 expression inhibition by analyzing a series of 56 benign and malignant AT with molecular cytogenetic data; We measured the levels of expression of HMGA2 mRNA and of eight members of the let-7 microRNA family using quantitative RT-PCR and expression of HMGA2 protein using immunohistochemistry; Although overexpression of both HMGA2 mRNA and protein in a majority of ordinary lipomas without HMGA2 structural rearrangement may have suggested a potential role for let-7 microRNAs we did not observe a significant link with let-7 inhibition in such cases	;;;tumorigenesis;;;;malignant trasformation	gastric cancer;gastric cancer;ovarian cancer;esophageal cancer;esophageal cancer;lung squamous cell cancer;lung cancer;sarcoma
hsa-let-7b-3p	HMGA2	0.120166961637302	0.299224004314356	4.45669314139083	6.73354275393639e-30	mirMAP	-0.31912084584957	0.0436600906127955	20949044;18413822;23073586;21598109;24612219;23700794;21412931	Since let-7 miRNAs generally play a tumor-suppressive role as targeting oncogenes such as RAS and HMGA2 our results suggest that AZ-P7a cells release let-7 miRNAs via exosomes into the extracellular environment to maintain their oncogenesis;Recent studies report that HMGA2 is negatively regulated by the let-7 microRNA miRNA family; However no studies have examined the clinical significance of HMGA2 and its relationship to the let-7 miRNA family in gastric cancer; We also did an association study comparing HMGA2 expression and let-7 miRNA family expression in gastric cancer; Furthermore our findings suggest that HMGA2 is negatively regulated by the let-7 miRNA family in human gastric cancer;HMGA2 mRNA and let-7 family microRNA were detected by real time fluorescent quantitative reverse transcription polymerase chain reaction in the corresponding frozen tissues; All let-7 family members were detectable in all ovarian cancer samples and their expression were inversely correlated with HMGA2 mRNA expression r=-0.305P<0.05; The downregulation of let-7 is but not the only mechanism of HMGA2 overexpression in serous ovarian cancer;Role of microRNA let 7 and effect to HMGA2 in esophageal squamous cell carcinoma; To investigated the role of microRNA miRNA let-7 and its regulation on high mobility group A2 HMGA2 protein expression in esophageal squamous cell carcinoma ESCC; To evaluate the role of let-7 and HMGA2 cell proliferations were analyzed with synthetic let-7 mimics- or its inhibitor-transfected cells; The transcription of let-7 inversely correlated with HMGA2 protein; The present results demonstrated that let-7 and HMGA2 involved in ESCC carcinogenesis;HMGA2 is down regulated by microRNA let 7 and associated with epithelial mesenchymal transition in oesophageal squamous cell carcinomas of Kazakhs; To investigate the expression of let-7 and its regulation of high-mobility group A2 protein HMGA2 and to verify the relationship between let-7 HMGA2 and the process of epithelial-mesenchymal transition EMT in oesophageal squamous cell carcinomas OSCC of Kazakh patients; Let-7 could repress expression of HMGA2 after co-transfection with let-7 and HMGA2 P = 0.002; Moreover let-7 expression was observed less frequently P = 2.0 × 10-8  and HMGA2 expression more frequently P = 1.0 × 10-10  in OSCC than in normal adjacent tissues; and let-7 expression was observed less frequently in OSCC from Kazakh patients than in those from Han and Uygur patients P = 0.041; There was a reverse correlation between expression of let-7 and HMGA2 P = 0.018; Expression of let-7 can suppress cell proliferation by acting directly on regulation of HMGA2 in OSCC;MiR-98 a member in the let-7 family acts as a negative regulator in the expression of HMGA2 high mobility group A2 oncogene and it has been shown to have a nearly 3-fold decrease in A549/DDP cells;Let 7 microRNA and HMGA2 levels of expression are not inversely linked in adipocytic tumors: analysis of 56 lipomas and liposarcomas with molecular cytogenetic data; The aim of our study was first to assess the role of HMGA2 expression in the pathogenesis of adipocytic tumors AT and second to seek a potential correlation between overexpression of HMGA2 and let-7 expression inhibition by analyzing a series of 56 benign and malignant AT with molecular cytogenetic data; We measured the levels of expression of HMGA2 mRNA and of eight members of the let-7 microRNA family using quantitative RT-PCR and expression of HMGA2 protein using immunohistochemistry; Although overexpression of both HMGA2 mRNA and protein in a majority of ordinary lipomas without HMGA2 structural rearrangement may have suggested a potential role for let-7 microRNAs we did not observe a significant link with let-7 inhibition in such cases	;;;tumorigenesis;;;malignant trasformation	gastric cancer;gastric cancer;ovarian cancer;esophageal cancer;esophageal cancer;lung cancer;sarcoma
hsa-let-7b-5p	HMGA2	-0.2489842756826	0.0211384499461719	4.45669314139083	6.73354275393639e-30	miRNAWalker2_validate;miRTarBase;MirTarget	-0.691388425103243	4.04231698451336e-05	20949044;18413822;23073586;21598109;24612219;23700794;21412931	Since let-7 miRNAs generally play a tumor-suppressive role as targeting oncogenes such as RAS and HMGA2 our results suggest that AZ-P7a cells release let-7 miRNAs via exosomes into the extracellular environment to maintain their oncogenesis;Recent studies report that HMGA2 is negatively regulated by the let-7 microRNA miRNA family; However no studies have examined the clinical significance of HMGA2 and its relationship to the let-7 miRNA family in gastric cancer; We also did an association study comparing HMGA2 expression and let-7 miRNA family expression in gastric cancer; Furthermore our findings suggest that HMGA2 is negatively regulated by the let-7 miRNA family in human gastric cancer;HMGA2 mRNA and let-7 family microRNA were detected by real time fluorescent quantitative reverse transcription polymerase chain reaction in the corresponding frozen tissues; All let-7 family members were detectable in all ovarian cancer samples and their expression were inversely correlated with HMGA2 mRNA expression r=-0.305P<0.05; The downregulation of let-7 is but not the only mechanism of HMGA2 overexpression in serous ovarian cancer;Role of microRNA let 7 and effect to HMGA2 in esophageal squamous cell carcinoma; To investigated the role of microRNA miRNA let-7 and its regulation on high mobility group A2 HMGA2 protein expression in esophageal squamous cell carcinoma ESCC; To evaluate the role of let-7 and HMGA2 cell proliferations were analyzed with synthetic let-7 mimics- or its inhibitor-transfected cells; The transcription of let-7 inversely correlated with HMGA2 protein; The present results demonstrated that let-7 and HMGA2 involved in ESCC carcinogenesis;HMGA2 is down regulated by microRNA let 7 and associated with epithelial mesenchymal transition in oesophageal squamous cell carcinomas of Kazakhs; To investigate the expression of let-7 and its regulation of high-mobility group A2 protein HMGA2 and to verify the relationship between let-7 HMGA2 and the process of epithelial-mesenchymal transition EMT in oesophageal squamous cell carcinomas OSCC of Kazakh patients; Let-7 could repress expression of HMGA2 after co-transfection with let-7 and HMGA2 P = 0.002; Moreover let-7 expression was observed less frequently P = 2.0 × 10-8  and HMGA2 expression more frequently P = 1.0 × 10-10  in OSCC than in normal adjacent tissues; and let-7 expression was observed less frequently in OSCC from Kazakh patients than in those from Han and Uygur patients P = 0.041; There was a reverse correlation between expression of let-7 and HMGA2 P = 0.018; Expression of let-7 can suppress cell proliferation by acting directly on regulation of HMGA2 in OSCC;MiR-98 a member in the let-7 family acts as a negative regulator in the expression of HMGA2 high mobility group A2 oncogene and it has been shown to have a nearly 3-fold decrease in A549/DDP cells;Let 7 microRNA and HMGA2 levels of expression are not inversely linked in adipocytic tumors: analysis of 56 lipomas and liposarcomas with molecular cytogenetic data; The aim of our study was first to assess the role of HMGA2 expression in the pathogenesis of adipocytic tumors AT and second to seek a potential correlation between overexpression of HMGA2 and let-7 expression inhibition by analyzing a series of 56 benign and malignant AT with molecular cytogenetic data; We measured the levels of expression of HMGA2 mRNA and of eight members of the let-7 microRNA family using quantitative RT-PCR and expression of HMGA2 protein using immunohistochemistry; Although overexpression of both HMGA2 mRNA and protein in a majority of ordinary lipomas without HMGA2 structural rearrangement may have suggested a potential role for let-7 microRNAs we did not observe a significant link with let-7 inhibition in such cases	;;;tumorigenesis;;;malignant trasformation	gastric cancer;gastric cancer;ovarian cancer;esophageal cancer;esophageal cancer;lung cancer;sarcoma
hsa-let-7c-5p	HMGA2	-2.07953368242668	3.46048888391218e-23	4.45669314139083	6.73354275393639e-30	miRNAWalker2_validate;miRTarBase;MirTarget	-0.806534505069892	1.97059168844052e-24		NA	NA	NA
hsa-let-7f-5p	HMGA2	-0.441845198213823	0.00242957484218694	4.45669314139083	6.73354275393639e-30	miRNAWalker2_validate;MirTarget	-0.347051022079953	0.00531020669613986		NA	NA	NA
hsa-let-7g-5p	HMGA2	-0.250780249469264	0.00939610188330072	4.45669314139083	6.73354275393639e-30	miRNAWalker2_validate;miRTarBase;MirTarget	-0.74644926991967	7.75936678734911e-05	21472347;18308936	Furthermore K-Ras and HMGA2 are well known as targets of let-7g; In this study we evaluated the potential role of precursor pre-let-7g in lung cancer cell metastasis focusing on the two targets of let-7g HMGA2 and K-Ras;In let-7g expressing tumors reductions in Ras family and HMGA2 protein levels were detected; Ectopic expression of K-RasG12D largely rescued let-7g mediated tumor suppression whereas ectopic expression of HMGA2 was less effective	metastasis;	lung cancer;lung cancer
hsa-miR-125b-2-3p	HMGA2	-1.87765459914049	1.24704155651697e-13	4.45669314139083	6.73354275393639e-30	mirMAP	-0.599672774947008	6.43066358581415e-19		NA	NA	NA
hsa-miR-125b-5p	HMGA2	-0.993460109818276	5.07736727659894e-12	4.45669314139083	6.73354275393639e-30	miRNAWalker2_validate;miRTarBase	-0.872723332276466	6.10970209720732e-13		NA	NA	NA
hsa-miR-148a-5p	HMGA2	-1.00478606532747	1.38045244999229e-07	4.45669314139083	6.73354275393639e-30	mirMAP	-0.523038517814871	1.85520060076771e-08		NA	NA	NA
hsa-miR-195-3p	HMGA2	-0.624259620429699	0.000164279659144497	4.45669314139083	6.73354275393639e-30	mirMAP	-0.725637328373556	1.63618840176472e-11		NA	NA	NA
hsa-miR-195-5p	HMGA2	-1.8367376818177	6.9944883988895e-31	4.45669314139083	6.73354275393639e-30	MirTarget	-0.819173795732359	5.773484084711e-15		NA	NA	NA
hsa-miR-199a-5p	HMGA2	-0.364835768178638	0.0435119211101981	4.45669314139083	6.73354275393639e-30	miRanda	-0.275403367704305	0.00610524579591463		NA	NA	NA
hsa-miR-199b-5p	HMGA2	-1.08432682485992	7.68241801134089e-10	4.45669314139083	6.73354275393639e-30	miRanda	-0.406043346525521	5.75094161893386e-05		NA	NA	NA
hsa-miR-20b-5p	HMGA2	0.345967670847176	0.232014828043601	4.45669314139083	6.73354275393639e-30	miRNATAP	-0.307766242278935	7.47592102369256e-07		NA	NA	NA
hsa-miR-23b-3p	HMGA2	-0.497563803223134	3.31483353357535e-05	4.45669314139083	6.73354275393639e-30	mirMAP	-1.06526143657057	6.29790009739926e-13		NA	NA	NA
hsa-miR-26a-5p	HMGA2	-1.09269574587169	1.24020612216319e-22	4.45669314139083	6.73354275393639e-30	miRNAWalker2_validate;miRTarBase;miRNATAP	-1.05161832046561	8.02917727136433e-12	24682444	Furthermore we demonstrated that high mobility group AT-hook 2 HMGA2 was a direct target of miR-26a; The results showed that HMGA2 mRNA levels and miR-26a levels were negatively correlated; In addition we confirmed that reintroduction of HMGA2 antagonized the inhibition of miR-26a to GBC cell proliferation and all these effects were achieved through the cell cycle; Together all these results suggest that miR-26a expression contributes to GBC proliferation by targeting HMGA2 miR-26a shows promise as a prognosis factor and therapeutic target of GBC patients	worse prognosis	bladder cancer
hsa-miR-29b-2-5p	HMGA2	-0.502720326849742	0.000730448246894952	4.45669314139083	6.73354275393639e-30	mirMAP	-0.584885614571135	1.29765650281039e-06		NA	NA	NA
hsa-miR-30a-3p	HMGA2	-2.26144364746452	8.12421214153823e-31	4.45669314139083	6.73354275393639e-30	MirTarget	-0.514231578446967	2.24499877403303e-09		NA	NA	NA
hsa-miR-30a-5p	HMGA2	-1.79779915425811	1.93360169837799e-26	4.45669314139083	6.73354275393639e-30	mirMAP	-0.615108101185708	1.0013099700026e-09		NA	NA	NA
hsa-miR-30b-5p	HMGA2	-0.400238605368173	0.00346540992719245	4.45669314139083	6.73354275393639e-30	mirMAP	-0.391922741594788	0.00311827075770731		NA	NA	NA
hsa-miR-30c-5p	HMGA2	0.021222006155897	0.886366656528128	4.45669314139083	6.73354275393639e-30	mirMAP	-0.280609657396151	0.0223399458123554		NA	NA	NA
hsa-miR-30d-3p	HMGA2	-0.577371911152798	2.02950840095287e-06	4.45669314139083	6.73354275393639e-30	MirTarget	-0.577014479735653	0.000102105825776101		NA	NA	NA
hsa-miR-30d-5p	HMGA2	-0.38399848121878	0.000171129616944749	4.45669314139083	6.73354275393639e-30	mirMAP	-0.916535323743468	2.11860119813698e-07		NA	NA	NA
hsa-miR-30e-3p	HMGA2	-0.890635378639789	1.65740480611339e-16	4.45669314139083	6.73354275393639e-30	MirTarget	-1.37773413661885	4.43836162945141e-18		NA	NA	NA
hsa-miR-30e-5p	HMGA2	-1.02114836019762	6.81961221797866e-17	4.45669314139083	6.73354275393639e-30	mirMAP	-1.27539430690017	5.81942504308282e-20		NA	NA	NA
hsa-miR-32-5p	HMGA2	-0.317310201890053	0.0102525324475293	4.45669314139083	6.73354275393639e-30	miRNATAP	-0.350374884334623	0.0175042753942361		NA	NA	NA
hsa-miR-326	HMGA2	-0.425943992128769	0.0415010315530797	4.45669314139083	6.73354275393639e-30	miRNATAP	-0.203342537615888	0.0197442120534773		NA	NA	NA
hsa-miR-337-3p	HMGA2	-1.70091836051933	1.39844536073221e-13	4.45669314139083	6.73354275393639e-30	MirTarget;PITA	-0.221747768144724	0.00394222082620597		NA	NA	NA
hsa-miR-340-5p	HMGA2	-0.608415693437977	4.44345153563513e-05	4.45669314139083	6.73354275393639e-30	mirMAP	-0.340606377991935	0.00498062871245901		NA	NA	NA
hsa-miR-34a-5p	HMGA2	-0.117372471043915	0.364001947180738	4.45669314139083	6.73354275393639e-30	miRNAWalker2_validate	-0.562179871493631	6.3475156812021e-05	18803879	miR-34 targets Notch HMGA2 and Bcl-2 genes involved in the self-renewal and survival of cancer stem cells; Human gastric cancer Kato III cells with miR-34 restoration reduced the expression of target genes Bcl-2 Notch and HMGA2; The mechanism of miR-34-mediated suppression of self-renewal appears to be related to the direct modulation of downstream targets Bcl-2 Notch and HMGA2 indicating that miR-34 may be involved in gastric cancer stem cell self-renewal/differentiation decision-making	poor survival;differentiation	gastric cancer
hsa-miR-374a-3p	HMGA2	-0.299190081500425	0.00682975596757891	4.45669314139083	6.73354275393639e-30	miRNATAP	-0.416242795753572	0.0116620137907771		NA	NA	NA
hsa-miR-381-3p	HMGA2	-2.21357103508055	2.33039447871705e-24	4.45669314139083	6.73354275393639e-30	mirMAP	-0.230970155746285	0.00370009996135725		NA	NA	NA
hsa-miR-491-5p	HMGA2	-0.541680329196715	0.00135829217561865	4.45669314139083	6.73354275393639e-30	PITA;miRanda	-0.329740380355764	0.00325839492784468		NA	NA	NA
hsa-miR-497-5p	HMGA2	-0.966244470847844	5.26505649147857e-12	4.45669314139083	6.73354275393639e-30	MirTarget	-0.944887976209222	2.8689194152602e-14		NA	NA	NA
hsa-miR-532-5p	HMGA2	-0.021857649390892	0.830992272120134	4.45669314139083	6.73354275393639e-30	mirMAP	-0.583280932634989	0.00110658177646052		NA	NA	NA
hsa-miR-664a-3p	HMGA2	-0.256108763664991	0.0513188660751664	4.45669314139083	6.73354275393639e-30	mirMAP	-0.48225892689875	0.000489112416746478		NA	NA	NA
hsa-miR-664a-5p	HMGA2	-0.871809752100072	1.86842520324979e-08	4.45669314139083	6.73354275393639e-30	MirTarget	-0.557050731768997	1.32920444175119e-06		NA	NA	NA