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Title: Regulation of the P2X7R by microRNA-216b in human breast cancer

Highlights: • We suggest the expression level of miR-216b and P2X7R in breast cancer tissues and cell lines. • We demonstrated that miR-216b directly targets and inhibits P2X7R. • We suggested miR-216b can attenuate ATP/P2X7R signaling pathways and induced Bcl-2/caspase-3 pathway. - Abstract: Breast cancer is the most common cancer in women around the world. However, the molecular mechanisms underlying breast cancer pathogenesis are only partially understood. Here, in this study, we found that P2X7R was up-regulated and miR-216b was down-regulated in breast cancer cell lines and tissues. Using bioinformatic analysis and 3′UTR luciferase reporter assay, we determined P2X7R can be directly targeted by miR-216b, which can down-regulate endogenous P2X7R mRNA and protein levels. Ectopic expression of miR-216b mimics leads to inhibited cell growth and apoptosis, while blocking expression of the miR-216b results in increased cell proliferation. Furthermore, our findings demonstrate that knockdown of P2X7R promotes apoptosis in breast cancer cells through down-regulating Bcl-2 and increasing the cleavage caspase-3 protein level. Finally, we confirmed that down-regulation of miR-216b in breast cancer is inversely associated with P2X7R expression level. Together, these findings establish miR-216b as a novel regulator of P2X7R and a potential therapeutic target for breast cancer.
Authors:
 [1] ;  [2] ;  [3] ; ; ; ; ; ;  [1] ;  [4]
  1. Department of Breast and Thyroid, Jinan Military General Hospital, Jinan 250031, Shandong Province (China)
  2. Department of General Surgery, Jinan Military General Hospital, Jinan 250031, Shandong Province (China)
  3. Department of General Surgery, Shanghai Ninth People’s Hospital, Shanghai 200011 (China)
  4. Department of Oncology, Jinan Military General Hospital, Jinan 250031, Shandong Province (China)
Publication Date:
OSTI Identifier:
22416743
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 452; Journal Issue: 1; Other Information: Copyright (c) 2014 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANIMAL TISSUES; APOPTOSIS; ATP; BORON CHLORIDES; CELL PROLIFERATION; CHANNELING; HUMAN POPULATIONS; LUCIFERASE; MAMMARY GLANDS; MESSENGER-RNA; NEOPLASMS; PATHOGENESIS; WOMEN