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miR‐384 suppressed renal cell carcinoma cell proliferation and migration through targeting RAB23
Author(s) -
Yan Lihua,
Wu Kunxiang,
Du Feng,
Yin Xianzhe,
Guan Hongmei
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27180
Subject(s) - ectopic expression , cell growth , microrna , cell , cancer research , renal cell carcinoma , suppressor , cell cycle , biology , downregulation and upregulation , cell migration , microbiology and biotechnology , gene , pathology , medicine , genetics
microRNAs (miRNAs) are noncoding, short, and endogenous RNAs that play crucial roles in tumor progression at the post‐transcriptional level. Here, we studied the role of miR‐384 in the pathogenesis of renal cell carcinoma (RCC). We demonstrated that miR‐384 expression was downregulated in the RCC specimens compared with nontumor specimens. Moreover, we showed that RAB23 expression was upregulated in the RCC tissues compared with nontumor tissues. Furthermore, we demonstrated that low expression of miR‐384 was correlated with high levels of RAB23 in RCC tissues. We also demonstrated that the RAB23 was a direct target gene of miR‐384 in RCC cells. In addition, overexpression of miR‐384 suppressed RCC cell proliferation, cell cycle, and cell migration. Furthermore, ectopic expression of RAB23 promoted RCC cell proliferation, cell cycle, and cell migration. These data suggested that miR‐384 played a tumor suppressor microRNA in the development of RCC partly through inhibiting RAB23 expression.