Survivin gene RNA interference inhibits proliferation, induces apoptosis, and enhances radiosensitivity in HeLa cells

Hui Song1, Xiao-Yan Xin, Feng Xiao

  • 1Department of Obstetrics and Gynecology, Xijing Hospital, Fourth Military Medical University, Shannxi, Xi'an 710032, China. xiaofeng@fmmu.edu.cn

Abstract

Insights

RNA interference targeting the survivin gene significantly inhibits human cervical carcinoma cell proliferation and enhances radiosensitivity. This survivin gene RNAi strategy offers a potential approach for radiosensitization therapy in cervical cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy

Background:

  • Survivin, an inhibitor of apoptosis protein, is upregulated in human cervical carcinomas.
  • While survivin reduction can chemosensitize cells, its effect on radiosensitization is unclear.

Purpose of the Study:

  • To investigate the effect of survivin gene RNA interference (RNAi) on HeLa cervical carcinoma cell proliferation, apoptosis, and radiosensitivity.

Main Methods:

  • HeLa cells were transfected with a survivin-targeting siRNA vector (pSilencer2.1-s2) or a control vector.
  • Survivin mRNA and protein expression were analyzed using RT-PCR and Western blotting.
  • Cell proliferation, cell cycle distribution, apoptosis, and radiosensitivity were assessed using MTT assay, flow cytometry, and clonogenic survival assays, respectively.

Main Results:

  • Survivin gene RNAi significantly reduced survivin mRNA and protein levels in HeLa cells (inhibitory rates of 62.8% and 60.1%).
  • Cell proliferation was inhibited by up to 57.8%, with cells accumulating in the G(0)/G(1) phase and increased apoptosis (29.2%).
  • Radiosensitivity was significantly enhanced, with decreased cloning efficiency, D(0) (3.15), and D(q) (1.21), and radiation enhancement ratios of 2.01 and 1.77.

Conclusions:

  • Survivin gene RNAi effectively inhibits cervical carcinoma cell proliferation and enhances radiosensitivity.
  • Targeting survivin via RNAi presents a promising strategy for radiosensitization therapy in human cervical carcinomas.

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