[Selective apoptosis in HeLa cells induced by sodium butyrate and its mechanism]

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2003 Aug;25(4):401-5.
[Article in Chinese]

Abstract

Objective: To investigate apoptosis induced by sodium butyrate in cervix cancer cell line HeLa and primary human embryo lung fibroblasts and its mechanism.

Methods: Cell apoptosis was assessed by morphology, cell viability, DNA fragmentation, the percentage of sub-G1 cells and phosphatidylserine (PS) externalization. The effects of sodium butyrate on transcription of Bax and Bcl-2 was analyzed by RT-PCR.

Results: Sodium butyrate inhibited proliferation in a time and dose-dependant manner. The inhibition of proliferation in HeLa cells was more significant than that in primary human embryo lung fibroblasts. DNA fragmentation, sub-G1 peak and AnnexinV/PI by flow cytometry showed very high apoptosis rates in HeLa cells 72 hours after treated with sodium butyrate, while pretty low in primary human embryo lung fibroblasts. RT-PCR showed sodium butyrate had little effects on transcription of Bax and Bcl-2 in HeLa cells.

Conclusion: Sodium butyrate can induce apoptosis in HeLa cells without changing the expression of Bax and Bcl-2. Sodium butyrate comparatively has little effects on fibroblasts.

Publication types

  • Comparative Study
  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Butyrates / pharmacology*
  • Cell Division / drug effects
  • DNA Fragmentation
  • Female
  • Flow Cytometry
  • HeLa Cells
  • Humans
  • Proto-Oncogene Proteins / biosynthesis
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • bcl-2-Associated X Protein

Substances

  • Antineoplastic Agents
  • BAX protein, human
  • Butyrates
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein