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Reduction of protein kinase C α (PKC-α) promote apoptosis via down-regulation of Dicer in bladder cancer.

Abstract
In clinic, we examined the expression of protein kinase C (PKC)-α and Dicer in the samples of bladder cancer patients, and found that the two proteins have a line correlation. Our study confirmed this correlation existing by clearing the decreasing expression of Dicer after the PKC-α knockdown. Treatment of bladder cancer cell lines (T24, 5637) with the PKC-α or Dicer knockdown and the PKC inhibitors (Calphostin C and Gö 6976) can promote the apoptosis. Inhibition of PKC can increase the activities of caspase-3 and PARP, however, decrease the expression of Dicer. And knockdown of the PKC-α or Dicer can also activate the caspase-3 or the PARP. Considering the reduction of PKC-α can induce the Dicer down-regulation, we make the conclusion that the reduction of PKC-α can promote the apoptosis via the down-regulation of Dicer in bladder cancer.
AuthorsZhenming Jiang, Chuize Kong, Zhe Zhang, Yuyan Zhu, Yuxi Zhang, Xi Chen
JournalJournal of cellular and molecular medicine (J Cell Mol Med) Vol. 19 Issue 5 Pg. 1085-93 (May 2015) ISSN: 1582-4934 [Electronic] England
PMID25752336 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
Chemical References
  • Carbazoles
  • Enzyme Inhibitors
  • Naphthalenes
  • Go 6976
  • Poly(ADP-ribose) Polymerases
  • PRKCA protein, human
  • Protein Kinase C-alpha
  • Ribonuclease III
  • Caspase 3
  • calphostin C
Topics
  • Apoptosis (drug effects, genetics)
  • Blotting, Western
  • Carbazoles (pharmacology)
  • Caspase 3 (metabolism)
  • Cell Line, Tumor
  • Down-Regulation
  • Enzyme Inhibitors (pharmacology)
  • Fluorescent Antibody Technique
  • Humans
  • Naphthalenes (pharmacology)
  • Poly(ADP-ribose) Polymerases (metabolism)
  • Protein Kinase C-alpha (antagonists & inhibitors, genetics, metabolism)
  • RNA Interference
  • Reverse Transcriptase Polymerase Chain Reaction
  • Ribonuclease III (genetics, metabolism)
  • Urinary Bladder Neoplasms (genetics, metabolism, pathology)

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