miRNA	gene	miRNA_log2FC	miRNA_pvalue	gene_log2FC	gene_pvalue	interactions	correlation_beta	correlation_pvalue	PMID	evidence	outcome	cancer
hsa-miR-140-3p	KRAS	-1.25844395244141	5.29222651039892e-33	0.46818988509622	3.00748217900386e-10	MirTarget	-0.245149449217664	6.89860831179258e-27		NA	NA	NA
hsa-miR-143-3p	KRAS	-1.23248181631499	4.74160976678504e-28	0.46818988509622	3.00748217900386e-10	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.124135749972866	1.80319700574441e-08	22804917;27725862;19137007;26581910;23173124;26824186;21197560	In KRAS mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS;The expression of miR-143 is often down-regulated and it might play an important role by targeting KRAS in colorectal cancer CRC; Dual-luciferase reporter assays were performed to validate whether KRAS was regulated by miR-143; Dual-luciferase assays indicated that KRAS was a direct target of miR-143 as subsequently demonstrated by qPCR and western blot analysis showing that infection of SW480 cells with Ad-ZD55-miR-143 resulted in the down-regulation of KRAS at both mRNA and protein levels;Role of miR 143 targeting KRAS in colorectal tumorigenesis; In particular among a panel of presumed targets generated by in silico analysis that may interact with these aberrantly expressed miRNAs KRAS oncogene has been further experimentally validated as the target of miR-143; First an inverse correlation between KRAS protein and miR-143 in vivo was found; Second KRAS expression in Lovo cells was significantly abolished by treatment with miR-143 mimic whereas miR-143 inhibitor increased KRAS protein level; Third luciferase reporter assay confirmed that miR-143 directly recognize the 3'-untranslated region of KRAS transcripts; Finally inhibition of KRAS expression by miR-143 inhibits constitutive phosphorylation of ERK1/2; Taken together the present study provides the first evidences that miR-143 is significant in suppressing colorectal cancer cell growth through inhibition of KRAS translation;MicroRNA 143 replenishment re sensitizes colorectal cancer cells harboring mutant but not wild type KRAS to paclitaxel treatment; Our results showed that miR-143 but not let-7b increased sensitization of KRAS mutant tumor cells to paclitaxel; Furthermore transfection of miR-143 but not let-7b mimic negatively regulated the expression of mutant but not wild-type KRAS; Combination of miR-143 mimic and paclitaxel induced the onset of apoptosis and reverted in vitro metastatic properties migration and invasion in KRAS mutant tumor cells; MiR-143 thus can be used as a chemosensitizer for the treatment of KRAS mutant tumors and warrants further investigations in in vitro and pre-clinical in vivo models;In turn the level of miR-143 in CRC cells decreasing the amount of MACC1 metastasis-associated in colon cancer-1 and oncogenic KRAS protein may be utilized as a prognostic marker;Stable miR-143 or miR-145 overexpression increased cell sensitivity to cetuximab resulting in a significant increase of cetuximab-mediated ADCC independently of KRAS status;miR 143 decreases prostate cancer cells proliferation and migration and enhances their sensitivity to docetaxel through suppression of KRAS; The expression level of miR-143 and its target gene KRAS were measured by realtime PCR and western blotting respectively; Our results revealed an inverse correlation of expression between miR-143 and KRAS protein in prostate cancer samples Pearson's correlation scatter plots: R = -0.707 P < 0.05; These findings suggest that miR-143 plays an important role in prostate cancer proliferation migration and chemosensitivity by suppressing KRAS and subsequent inactivation of MAPK pathway which provides a potential development of a new approach for the treatment of prostate cancer	;;tumorigenesis;;metastasis;;	colorectal cancer;colorectal cancer;colorectal cancer;colorectal cancer;colorectal cancer;colon cancer;prostate cancer
hsa-miR-181a-5p	KRAS	0.635863607630183	6.72486918157744e-11	0.46818988509622	3.00748217900386e-10	miRNAWalker2_validate	-0.0863387786787699	0.000979915712483209	24098024;27517749;26124189	The KRAS mutational status was determined by pyrosequencing and miR-181a expression was measured by quantitative RT-PCR in CRC tumour tissue and corresponding non-neoplastic colon tissue;Here we report that miR-181a directly binds to 3'-untranslated regions UTRs; downregulates KRAS NRAS and MAPK1; and decreases AML growth; The delivery of miR-181a mimics to target AML cells using transferrin-targeting lipopolyplex nanoparticles NP increased mature miR-181a; downregulated KRAS NRAS and MAPK1; and resulted in decreased phosphorylation of the downstream RAS effectors;MiR 181a 5p inhibits cell proliferation and migration by targeting Kras in non small cell lung cancer A549 cells; Luciferase activity assay results demonstrated that two binding sites of Kras could be directly targeted by miR-181a-5p; Furthermore Kras was down-regulated by miR-181a-5p at both transcriptional and translational levels; SiRNA-mediated Kras down-regulation could mimic the effects of miR-181a-5p mimic in A549 cells; Our findings suggest that miR-181a-5p plays a potential role in tumor suppression by partially targeting Kras and has the potential therapeutic application in NSCLC patients	;;	colorectal cancer;acute myeloid leukemia;lung squamous cell cancer
hsa-miR-193a-5p	KRAS	-1.1508321886378	7.11949564429669e-37	0.46818988509622	3.00748217900386e-10	miRNATAP	-0.0674217780316105	0.0133283944906005		NA	NA	NA
hsa-miR-195-3p	KRAS	-1.49582726452416	6.53261924105147e-40	0.46818988509622	3.00748217900386e-10	mirMAP	-0.144084535908296	1.9114583860958e-11		NA	NA	NA
hsa-miR-199b-5p	KRAS	-1.37022396448377	3.25758057539223e-26	0.46818988509622	3.00748217900386e-10	miRanda;miRNATAP	-0.0743923623669612	0.000111044005365755	27517624	The miR-199b prognostic impact was particularly evident in both younger and KRAS wild-type subgroups		colorectal cancer
hsa-miR-217	KRAS	-0.616728851115349	8.64977119332241e-05	0.46818988509622	3.00748217900386e-10	miRNAWalker2_validate;miRTarBase;MirTarget;PITA;miRanda;miRNATAP	-0.0521976363108665	0.00137710732177109	25234467;26062553	The overexpression of miR-217 significantly inhibited the proliferation migration and invasion as well as promoted the apoptosis of lung cancer cells by targeting KRAS; In conclusion miR-217 suppresses tumour development in lung cancer by targeting KRAS and enhances cell sensitivity to cisplatin;Quercetin Enhances Cisplatin Sensitivity of Human Osteosarcoma Cells by Modulating microRNA 217 KRAS Axis; Expression of miR-217 was upregulated after quercetin and/or cisplatin treatment while its target KRAS was downregulated both at mRNA and protein levels	;	lung cancer;sarcoma
hsa-miR-30b-5p	KRAS	-0.46540603860146	2.4709940429591e-05	0.46818988509622	3.00748217900386e-10	mirMAP;miRNATAP	-0.0786518426716973	0.000718627065609599		NA	NA	NA
hsa-miR-30d-5p	KRAS	-0.247082219011045	0.00406717930063148	0.46818988509622	3.00748217900386e-10	mirMAP;miRNATAP	-0.13177346252977	1.09256098608436e-05		NA	NA	NA
hsa-miR-335-3p	KRAS	-1.88448538773649	2.09538234398335e-32	0.46818988509622	3.00748217900386e-10	mirMAP	-0.0557760374126412	0.000326581799999939		NA	NA	NA
hsa-miR-495-3p	KRAS	-1.67685437612894	1.70634429769052e-34	0.46818988509622	3.00748217900386e-10	mirMAP	-0.0517519009363879	0.00419366977097126		NA	NA	NA
hsa-miR-502-3p	KRAS	0.11461741546458	0.276553832470138	0.46818988509622	3.00748217900386e-10	MirTarget;PITA;miRNATAP	-0.0556183010871932	0.0235163097973418		NA	NA	NA
hsa-miR-532-5p	KRAS	0.0386976222860582	0.682018574136515	0.46818988509622	3.00748217900386e-10	MirTarget;PITA;miRNATAP	-0.0679560683201416	0.0131684908416608		NA	NA	NA
hsa-miR-542-3p	KRAS	0.568822103820889	8.5699075257651e-07	0.46818988509622	3.00748217900386e-10	miRanda	-0.123003016716369	2.33095765684339e-08		NA	NA	NA
hsa-miR-584-5p	KRAS	-1.75458362433615	2.80754771470968e-33	0.46818988509622	3.00748217900386e-10	MirTarget	-0.0534907322311453	0.00156020927109316		NA	NA	NA