title: miR-106a* inhibits the proliferation of renal carcinoma cells by targeting IRS-2.
abstract: MicroRNAs play critical roles in the development and progression of human cancers. Although it has been reported that miR-106a* is downregulated in follicular lymphoma, its role in renal cell carcinoma (RCC) remains unknown. This study investigated the expression and role of miR-106a* in human RCC. Our results showed that the miR-106a* expression decreased dramatically in clinical RCC tissues and cell lines. In vitro, overexpression of miR-106a* suppressed RCC cell proliferation and S/G2 transition, whereas inhibition of miR-106a* promoted cell proliferation and S/G2 transition. It was also found that miR-106a* expression was inversely correlated with the expression of insulin receptor substrate 2 (IRS-2). IRS-2 was determined to be a direct target of miR-106a* by a luciferase reporter assay. Importantly, silencing IRS-2 resulted in the same biologic effects as those of miR-106a* overexpression in RCC cells, including inhibition of RCC cell proliferation and triggering of S/G2 cell cycle arrest with inhibition of the PI3K/Akt signaling pathway. These results indicate that miR-106a* affects RCC progression by targeting IRS-2 with suppression of the PI3K/Akt signaling pathway in RCC cells. The findings suggest miR-106a* as a novel strategy for RCC treatment.
authors.affiliation: Department of Urology, the Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, People's Republic of China.|Department of Urology, Affiliated Hospital, Yan'an University, Yan'an City, Shanxi, 716000, People's Republic of China.
authors.forename: Yadong
authors.initials: Y
authors.lastname: Ma
authors.affiliation: Department of Urology, Affiliated Hospital, Yan'an University, Yan'an City, Shanxi, 716000, People's Republic of China.
authors.forename: Hongyi
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Urology, Affiliated Hospital, Yan'an University, Yan'an City, Shanxi, 716000, People's Republic of China.
authors.forename: Xiaolong
authors.initials: X
authors.lastname: He
authors.affiliation: Department of Urology, Affiliated Hospital, Yan'an University, Yan'an City, Shanxi, 716000, People's Republic of China.
authors.forename: Hongxiong
authors.initials: H
authors.lastname: Song
authors.affiliation: Department of Urology, Affiliated Hospital, Yan'an University, Yan'an City, Shanxi, 716000, People's Republic of China.
authors.forename: Yayong
authors.initials: Y
authors.lastname: Qiang
authors.affiliation: Department of Urology, Affiliated Hospital, Yan'an University, Yan'an City, Shanxi, 716000, People's Republic of China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Urology, Affiliated Hospital, Yan'an University, Yan'an City, Shanxi, 716000, People's Republic of China.
authors.forename: Jixue
authors.initials: J
authors.lastname: Gao
authors.affiliation: Department of Urology, the Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, People's Republic of China. wangziming201415@126.com.
authors.forename: Ziming
authors.initials: Z
authors.lastname: Wang
mesh_terms: D000328:Adult; D000368:Aged; D002292:Carcinoma, Renal Cell / Q000235:genetics* / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D055504:Insulin Receptor Substrate Proteins / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D035683:MicroRNAs / Q000096:biosynthesis / Q000235:genetics*; D008875:Middle Aged; D051058:Oncogene Protein v-akt / Q000235:genetics; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics
chemical_list: C526297:IRS2 protein, human; D055504:Insulin Receptor Substrate Proteins; C542541:MIRN106 microRNA, human; D035683:MicroRNAs; D019869:Phosphatidylinositol 3-Kinases; D051058:Oncogene Protein v-akt
keywords: Insulin receptor substrates 2; PI3K/Akt signaling pathway; Proliferation; Renal cell carcinoma; miR-106a*