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Ribosomal protein small subunit 15A (RPS15A) inhibits the apoptosis of breast cancer MDA‐MB‐231 cells via upregulating phosphorylated ERK1/2, Bad, and Chk1
Author(s) -
Kong Lingsuo,
Wei Qing,
Hu Xianwen,
Chen Lanren,
Li Juan
Publication year - 2020
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.29304
Subject(s) - gene knockdown , apoptosis , gene silencing , small hairpin rna , cancer research , microbiology and biotechnology , messenger rna , phosphorylation , cell growth , immunohistochemistry , chemistry , biology , immunology , gene , biochemistry
Aim To detect the expression and identify the role of Ribosomal protein S15A (RPS15A) in human breast cancer (BC). Methods Immunohistochemistry (IHC) was carried out for detecting the levels of RPS15A protein. Quantitative PCR was used to evaluate the mRNA level of RPS15A in one normal breast and three BC cell lines. Lentivirus‐mediated shRNA targeting RPS15A was designed to investigate the impact of silencing RPS15A in MDA‐MB‐231 cell. Results Higher RPS15A expression was detected in tumor tissues than in para‐cancer tissues, and higher RPS15A expression was related to larger tumor size and higher TNM stage. Also, RPS15A mRNA expression in all three BC cell lines was higher than that in normal breast cell (all P < .005). Further, RPS15A knockdown significantly suppressed MDA‐MB‐231 cell proliferation and induced apoptosis. Moreover, RPS15A knockdown increased the caspase‐3/‐7 activity, and suppressed the phosphorylated levels of ERK1/2, Bad, and Chk1 (all P < .01). Conclusion RPS15A inhibits apoptosis via upregulating phosphorylated ERK1/2, Bad, and Chk1 in MDA‐MB‐231 cell line.