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Knock-down of NDRG2 sensitizes cervical cancer Hela cells to cisplatin through suppressing Bcl-2 expression

Junye Liu1, Le Yang, Jian Zhang

  • 1Department of Radiation Medicine, Fourth Military Medical University, Xi'an, China.

BMC Cancer
|August 28, 2012
PubMed
Abstract

Insights

Down-regulating NDRG2 (N-Myc downstream regulated gene 2) enhances cervical cancer Hela cells' sensitivity to cisplatin chemotherapy. This occurs by increasing apoptosis via the miR-15b/miR-16 pathway, which downregulates Bcl-2 protein expression.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • NDRG2 (N-Myc downstream regulated gene 2) is implicated in stress response, differentiation, and tumor suppression.
  • NDRG2 expression significantly increases in cervical cancer Hela cells treated with cisplatin.
  • This observation prompted an investigation into NDRG2's role in Hela cell chemosensitivity.

Purpose of the Study:

  • To evaluate the role of NDRG2 in cisplatin chemosensitivity of cervical cancer Hela cells.
  • To elucidate the molecular mechanisms underlying NDRG2's influence on chemosensitivity.
  • To determine if NDRG2 modulation affects cisplatin-induced apoptosis and related protein expression.

Main Methods:

  • RNA interference was used to down-regulate NDRG2 expression in Hela cells.
  • RT-PCR and Western blot analyzed NDRG2, Bcl-2, and Bax expression.
  • Real-time PCR quantified miR-15b and miR-16 levels.
  • MTT assays assessed drug sensitivity, colony-forming assays evaluated cloning efficiency, and flow cytometry detected apoptosis.

Main Results:

  • Suppression of NDRG2 sensitized Hela cells to cisplatin in vitro.
  • NDRG2 down-regulation promoted cisplatin-induced apoptosis without affecting colony-forming ability.
  • Inhibition of NDRG2 led to decreased Bcl-2 protein levels, but not mRNA levels.
  • miR-15b and miR-16 were significantly up-regulated in NDRG2-suppressed Hela cells.

Conclusions:

  • Down-regulation of NDRG2 enhances Hela cell sensitivity to cisplatin.
  • This sensitization is mediated by the inhibition of Bcl-2 protein expression.
  • Upregulation of miR-15b and miR-16 likely mediates the observed effects on Bcl-2.

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