4.4 Article

RPS7 promotes cell migration through targeting epithelial-mesenchymal transition in prostate cancer

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.urolonc.2019.01.011

关键词

RPS7; EMT; Cell migration; Prostate cancer

资金

  1. National Natural Science Foundation of China [81402124, 81472416, 21577097]
  2. Strategic Priority Research Program of the Chinese Academy of Sciences [XDB14000000]

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Objectives: Small ribosomal protein subunit 7 (RPS7) is an important structural components of the ribosome involved in protein synthesis, previous studies demonstrated that RPS7 was associated with several malignancies, but the role of RPS7 in prostate cancer (PCa) remains unclear. To decipher such a puzzle, in the current study, we deciphered the role and mechanism of RPS7 during the progression of PCa. Material and Methods: In this study, the expression of mRNA was performed by quantitative real-time PCR. The protein level was identified by Western blotting. Kaplan-Meier survival analysis was demonstrated the relation between the abnormal expression of RPS7 mRNA and the overall survival. Cell proliferation was assessed by MTT assay and cell counting, meanwhile, cell migration was checked by transwell assay. Results: RPS7 is higher expressed in PCa (p < 0.001), and the overexpression of RPS7 is closely associated with poor outcome of PCa patients after radical prostatectomy (p < 0.001). Inhibition the expression of RPS7 with a specific RPS7 siRNA could markedly attenuate prostate tumor growth and migration (p < 0.05). Mechanistic data reveals that inhibition of RPS7 could up-regulate the epithelial protein marker, E-cadherin (p < 0.05), and down-regulate the mesenchymal protein markers, such as N-cadherin and Snail (p < 0.001). Conclusions: RPS7 is a newly verified tumor promoter in PCa, and promotes cell migration by targeting epithelial-to-mesenchymal transition pathway. Thus, inhibition of RPS7-epithelial to-mesenchymal transition signaling might represent a prospective approach toward limiting prostate tumor progression. (C) 2019 Elsevier Inc. All rights reserved.

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