Premium
MiR‐193a‐3p and miR‐224 mediate renal cell carcinoma progression by targeting alpha‐2,3‐sialyltransferase IV and the phosphatidylinositol 3 kinase/Akt pathway
Author(s) -
Pan Yue,
Hu Jialei,
Ma Jia,
Qi Xia,
Zhou Huimin,
Miao Xiaoyan,
Zheng Wei,
Jia Li
Publication year - 2018
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.22826
Subject(s) - biology , protein kinase b , cancer research , pi3k/akt/mtor pathway , cell growth , metastasis , microrna , cell culture , kinase , signal transduction , cancer , microbiology and biotechnology , biochemistry , gene , genetics
Tumor metastasis is a major cause of cancer‐related death in renal cell carcinoma (RCC). MicroRNAs (miRNAs) have been widely known to modulate proliferation invasion, metastasis, and apoptosis of cancer cells. In this study, we aimed to investigate the function and novel target of miR‐193a‐3p and miR‐224 in RCC. The levels of miR‐193a‐3p and miR‐224 were significantly increased in RCC tissues and RCC cell lines. Alpha‐2,3‐Sialyltransferase IV (ST3GalIV) was highly expressed in adjacent nontumor tissues and human normal proximal tubular cell line HK‐2 compared to RCC tissues and cell lines. ST3GalIV expression was negatively correlated with miR‐193a‐3p and miR‐224. Further analysis indicated that miR‐193a‐3p and miR‐224 directly targeted ST3GalIV. MiR‐193a‐3p and miR‐224 increased cell proliferation and migration by directly inhibiting ST3GalIV, and this effect was reversed by co‐transfection with ST3GalIV in vitro. Overexpression of miR‐193a‐3p and miR‐224 increased RCC cell proliferation in vivo. Furthermore, the phosphatidylinositol 3 kinase (PI3K)/Akt pathway was mediated by miR‐193a‐3p and miR‐224 in RCC cell lines. Collectively, these results suggested that miR‐193a‐3p and miR‐224 played an important role in regulation of RCC by targeting ST3GalIV via PI3K/Akt pathway.