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Effect of autophagy-related beclin1 on sensitivity of cisplatin-resistant ovarian cancer cells to chemotherapeutic agents.

Abstract
The purpose of the study was to determine the effects of autophagy related gene Beclin1 at different levels of expression on the sensitivity of cisplatin-resistant ovarian cancer cells (SKOV3/DDP) to different chemotherapeutics. In pSUPER-Beclin1 transfected cells, real-time fluorescence quantitative RT-PCR and Western blot analysis showed that expression was significantly inhibited. Flow cytometry revealed that the mean fluorescence intensity (MDC), reflecting autophagy, and cells in the G0/G1 phase were markedly reduced. When compared with the blank control group, inhibition of Beclin1 expression in SKOV3/DDP cells not only increased the rate of apoptosis following treatment with chemotherapeutics, but also increased the sensitivity. These findings suggest that Beclin1 expression plays an important role in chemotherapeutic agent-induced death of SKOV3/DDP cells. Inhibition of autophagy related gene Beclin1 expression in SKOV3/DDP cells may increase the rate of apoptosis and elevate the sensitivity to chemotherapeutics.
AuthorsYang Sun, Jia-Hua Liu, Long Jin, Yu-Xia Sui, Li-Li Han, Yin Huang
JournalAsian Pacific journal of cancer prevention : APJCP (Asian Pac J Cancer Prev) Vol. 16 Issue 7 Pg. 2785-91 ( 2015) ISSN: 2476-762X [Electronic] Thailand
PMID25854363 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antineoplastic Agents
  • Apoptosis Regulatory Proteins
  • BECN1 protein, human
  • Beclin-1
  • Membrane Proteins
  • RNA, Messenger
  • Cisplatin
Topics
  • Antineoplastic Agents (pharmacology)
  • Apoptosis (drug effects)
  • Apoptosis Regulatory Proteins (genetics, metabolism)
  • Autophagy (drug effects)
  • Beclin-1
  • Blotting, Western
  • Cell Cycle (drug effects)
  • Cell Proliferation (drug effects)
  • Cisplatin (pharmacology)
  • Drug Resistance, Neoplasm
  • Female
  • Flow Cytometry
  • Humans
  • Immunoenzyme Techniques
  • Membrane Proteins (genetics, metabolism)
  • Ovarian Neoplasms (drug therapy, metabolism, pathology)
  • RNA, Messenger (genetics)
  • Real-Time Polymerase Chain Reaction
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Cells, Cultured

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