BTG1 potentiates apoptosis and suppresses proliferation in renal cell carcinoma by interacting with PRMT1
Author(s) -
Chunhui Liu,
Tao Tao,
Bin Xu,
Kai Lü,
Lei Zhang,
Liang Jiang,
Shuqiu Chen,
Dachuang Liu,
Xiaowen Zhang,
Nihao Cao,
Ming Chen
Publication year - 2015
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2015.3293
Subject(s) - cell cycle , cell growth , apoptosis , oncogene , biology , cell , cancer research , downregulation and upregulation , cell cycle checkpoint , renal cell carcinoma , microbiology and biotechnology , medicine , gene , genetics
B-cell translocation gene 1 (BTG1) is a member of the BTG/transducer of Erb family. BTG1 regulates cell cycle progression, inhibits proliferation, promotes apoptosis and stimulates cellular differentiation in multiple cell types. However, the functions of BTG1 in renal cell carcinoma (RCC) remain unclear. Therefore, the present study investigated the role of BTG1 in RCC tissue samples and 786-O RCC cells. RCC tissues and cells exhibited significantly weaker BTG1 protein and mRNA expression compared with para-carcinoma control tissues (P<0.05). Upregulated BTG1 expression induced significant G0/G1 cell cycle arrest, apoptosis and inhibition of cell proliferation in 786-O cells (P<0.05). Furthermore, BTG1 interacted with protein arginine N-methyltransferase 1 (PRMT1), and blocking the action of PRMT1 in 786-O cells resulted in inhibition of BTG1 function. These findings indicate that BTG1 may inhibit cell growth and promote apoptosis by interacting with PRMT1 in RCC; the identification of this mechanism may aid in the production of novel therapies for RCC.
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