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Biochem Biophys Res Commun. 2014 Sep 12;452(1):197-204. doi: 10.1016/j.bbrc.2014.07.101. Epub 2014 Jul 28.

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

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  • 1Department of Breast and Thyroid, Jinan Military General Hospital, Jinan 250031, Shandong Province, China.
  • 2Department of General Surgery, Jinan Military General Hospital, Jinan 250031, Shandong Province, China.
  • 3Department of General Surgery, Shanghai Ninth People's Hospital, Shanghai 200011, China.
  • 4Department of Oncology, Jinan Military General Hospital, Jinan 250031, Shandong Province, China. Electronic address:


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.

Copyright © 2014. Published by Elsevier Inc.


Apoptosis; Bcl-2; Breast cancer; Caspase-3; P2X7R; miR-216b

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