miRNA	gene	miRNA_log2FC	miRNA_pvalue	gene_log2FC	gene_pvalue	interactions	correlation_beta	correlation_pvalue	PMID	evidence	outcome	cancer
hsa-miR-103a-3p	SMAD7	0.538497806383155	1.88134691850591e-05	-1.03334261220629	1.40098151909512e-11	miRNAWalker2_validate	-0.175550659410964	0.00233649911608848		NA	NA	NA
hsa-miR-106a-5p	SMAD7	1.3902608059488	6.07931522284525e-05	-1.03334261220629	1.40098151909512e-11	miRNATAP	-0.126098371918768	2.91821282197453e-08		NA	NA	NA
hsa-miR-106b-5p	SMAD7	1.47447672652218	1.32004094930462e-13	-1.03334261220629	1.40098151909512e-11	miRNATAP	-0.20184823937347	6.73156217337974e-09	27619676;25286029;22286770	MiR 106b promotes migration and invasion through enhancing EMT via downregulation of Smad 7 in Kazakh's esophageal squamous cell carcinoma; To understand the regulation between miR-106b and Smad 7 qRT-PCR and western blot were performed; Smad 7 was confirmed as a downstream target of miR-106b in our experimental setting; Our results indicated that miR-106b can promote migration and invasion of ESCC cells through enhancing EMT process via downregulation of Smad 7 suggesting that miR-106b can be a potential molecular phenotype in ESCC metastases;Smad7 which inhibits transforming growth factor-β TGF-β/Smad signaling as a target of the miR-106b family was downregulated in CD44+ cells;The miR 106b 25 cluster targets Smad7 activates TGF β signaling and induces EMT and tumor initiating cell characteristics downstream of Six1 in human breast cancer	metastasis;;	esophageal cancer;gastric cancer;breast cancer
hsa-miR-16-5p	SMAD7	0.749619098384047	4.11649450706988e-06	-1.03334261220629	1.40098151909512e-11	miRNAWalker2_validate;MirTarget;miRNATAP	-0.146063396266522	0.000921870129280765		NA	NA	NA
hsa-miR-17-5p	SMAD7	2.07078488653279	2.77403038572568e-19	-1.03334261220629	1.40098151909512e-11	TargetScan;miRNATAP	-0.165693236232262	2.23894587820285e-08		NA	NA	NA
hsa-miR-182-5p	SMAD7	3.21839823004635	5.13049145201115e-39	-1.03334261220629	1.40098151909512e-11	miRNATAP	-0.134776563775354	3.86855719428812e-07		NA	NA	NA
hsa-miR-20a-5p	SMAD7	2.64649625616975	5.1469418982085e-27	-1.03334261220629	1.40098151909512e-11	miRNATAP	-0.134878840462214	8.34150952262662e-07		NA	NA	NA
hsa-miR-21-3p	SMAD7	2.54206008030157	1.11598785398763e-30	-1.03334261220629	1.40098151909512e-11	MirTarget	-0.116080725615902	0.000135903689078748	23372687;27185036;26531758	Furthermore the expression of MSH2 and SMAD7 two important molecules involving TGF-β pathway was restored following miR-21 knockdown in both MCF-7 and Hs578T breast cancer cells;MicroRNA 21 Regulates Non Small Cell Lung Cancer Cell Invasion and Chemo Sensitivity through SMAD7; We performed bioinformatics analyses on the binding of microRNA-21 miR-21 to the 3'-UTR of SMAD7 mRNA and verified the biological effects of this binding using promoter luciferase reporter assay; Furthermore expression of miR-21 was found to be inhibited by Carboplatin and bioinformatics analyses showed that miR-21 targeted the 3'-UTR of SMAD7 mRNA to inhibit its translation which was confirmed by luciferase reporter assay; Carboplatin may upregulate SMAD7 through suppression of miR-21 to inhibit TGFβ receptor signaling mediated NSCLC cell invasion;MicroRNA 21 induces breast cancer cell invasion and migration by suppressing smad7 via EGF and TGF β pathways; The present study was undertaken to determine the association of miR-21 smad7 EGF and TGF-β with breast cancer cell invasion and migration and to identify the molecular mechanisms involved using immunohistochemistry and western blot analysis; Smad7 was confirmed to be a direct target of miR-21 by luciferase reporter and western blot assays; The downregulation of smad7 by miR-21 or sismad7 enhanced EGF-dependent invasion and migration as well as TGF-β-dependent invasion and migration; The actions of miR-21 were abrogated by expressing a modified smad7 cDNA resistant to miR-21; In conclusion our results demonstrated that plasma miR-21 levels may serve as a diagnostic marker in breast cancers whereas miR-21 promotes breast cancer cell proliferation and invasion by suppressing smad7 which enhances EGF and TGF-β pathways	;;	breast cancer;lung squamous cell cancer;breast cancer
hsa-miR-21-5p	SMAD7	4.38165933891779	1.52536633902505e-92	-1.03334261220629	1.40098151909512e-11	miRNAWalker2_validate;MirTarget;miRNATAP	-0.148016758566167	4.47144478410339e-08	23372687;27185036;26531758	Furthermore the expression of MSH2 and SMAD7 two important molecules involving TGF-β pathway was restored following miR-21 knockdown in both MCF-7 and Hs578T breast cancer cells;MicroRNA 21 Regulates Non Small Cell Lung Cancer Cell Invasion and Chemo Sensitivity through SMAD7; We performed bioinformatics analyses on the binding of microRNA-21 miR-21 to the 3'-UTR of SMAD7 mRNA and verified the biological effects of this binding using promoter luciferase reporter assay; Furthermore expression of miR-21 was found to be inhibited by Carboplatin and bioinformatics analyses showed that miR-21 targeted the 3'-UTR of SMAD7 mRNA to inhibit its translation which was confirmed by luciferase reporter assay; Carboplatin may upregulate SMAD7 through suppression of miR-21 to inhibit TGFβ receptor signaling mediated NSCLC cell invasion;MicroRNA 21 induces breast cancer cell invasion and migration by suppressing smad7 via EGF and TGF β pathways; The present study was undertaken to determine the association of miR-21 smad7 EGF and TGF-β with breast cancer cell invasion and migration and to identify the molecular mechanisms involved using immunohistochemistry and western blot analysis; Smad7 was confirmed to be a direct target of miR-21 by luciferase reporter and western blot assays; The downregulation of smad7 by miR-21 or sismad7 enhanced EGF-dependent invasion and migration as well as TGF-β-dependent invasion and migration; The actions of miR-21 were abrogated by expressing a modified smad7 cDNA resistant to miR-21; In conclusion our results demonstrated that plasma miR-21 levels may serve as a diagnostic marker in breast cancers whereas miR-21 promotes breast cancer cell proliferation and invasion by suppressing smad7 which enhances EGF and TGF-β pathways	;;	breast cancer;lung squamous cell cancer;breast cancer
hsa-miR-25-3p	SMAD7	0.361927330834176	0.0163670566170988	-1.03334261220629	1.40098151909512e-11	miRNAWalker2_validate;MirTarget;miRNATAP	-0.174094723275729	0.000290663619179388	23435373	MicroRNA 25 functions as a potential tumor suppressor in colon cancer by targeting Smad7; Furthermore bioinformatic predictions and experimental validation were used to identify Smad7 as a direct target of miR-25; Functional reverse experiments indicated that the antitumor effects of miR-25 were probably mediated by its repression of Smad7; These results suggest that miR-25 may function as a tumor suppressor by targeting Smad7 in colon cancer		colon cancer
hsa-miR-590-3p	SMAD7	0.83851360565783	0.00129224433453587	-1.03334261220629	1.40098151909512e-11	miRanda	-0.165962125119586	3.92730078053594e-07		NA	NA	NA
hsa-miR-590-5p	SMAD7	2.07441240363458	4.95240551694843e-14	-1.03334261220629	1.40098151909512e-11	MirTarget;PITA;miRanda;miRNATAP	-0.147867429388902	2.34167471315949e-06		NA	NA	NA
hsa-miR-671-5p	SMAD7	2.24156654191798	2.10433241567652e-14	-1.03334261220629	1.40098151909512e-11	PITA	-0.121342374981944	1.85649329352746e-05		NA	NA	NA
hsa-miR-93-5p	SMAD7	1.50844106515467	1.83836866996875e-12	-1.03334261220629	1.40098151909512e-11	miRNATAP	-0.18049649492187	2.75705350284284e-08	25371073	Mothers against decapentaplegic homolog 7 Smad7 as an essential molecular protein for nuclear accumulation of β-catenin in the canonical Wnt signaling pathway is predicted as a putative target gene of miR-93 by the silico method and demonstrated that it may be suppressed by targeting its 3'UTR; These findings showed that miR-93 suppresses colorectal cancer development via downregulating Wnt/β-catenin at least in part by targeting Smad7		colorectal cancer
hsa-miR-98-5p	SMAD7	1.170602085804	1.09900501665229e-08	-1.03334261220629	1.40098151909512e-11	miRNAWalker2_validate	-0.152449463959285	1.67406719207547e-05		NA	NA	NA