[Study on the molecular mechanism of apoptosis in esophageal cancer cells induced by soybean isoflavone]

Zhonghua Liu Xing Bing Xue Za Zhi. 2003 Nov;24(11):1040-3.
[Article in Chinese]

Abstract

Objective: To investigate the function of apoptosis in esophageal cancer cells induced by soybean isoflavone, and the relation between this apoptosis and expression of bcl-2 and bax.

Methods: In vitro experiments, MTT assay was used to determine the cell growth inhibitory rate. Transmission electron microscope and TUNEL staining method were used to quantitatively and qualitatively detect the apoptosis status of esophageal cancer cell line EC-9706 before and after the soybean isoflavone treatment. Immunohistochemical staining and reverse transcription-polymerase chain reaction were used to detect the expression of apoptosis-regulated gene bcl-2 and bax.

Results: Soybean isoflavone inhibited the growth of esophageal cancer cell line EC-9706 in a dose- and time-dependent manner. Soybean isoflavone induced EC-9706 cells to undergo apoptosis with typically apoptotic characteristics, including morphological changes of chromatin condensation, chromatin crescent formation, nucleus fragmentation and apoptotic body formation by transmission electron microscope and staining positive cells, using TUNEL assay. Soybean isoflavone reduced the expression of apoptosis-regulated gene bcl-2, and improving the expression of apoptosis-regulated gene bax.

Conclusion: Soybean isoflavone seemed to be able to induce the apoptosis in esophageal cancer. This type of apoptosis might be mediated by down-expression of apoptosis-regulated gene bcl-2 and up-expression of apoptosis-regulated gene bax.

Publication types

  • English Abstract

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Cell Line, Tumor / drug effects
  • Dose-Response Relationship, Drug
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / metabolism
  • Esophageal Neoplasms / pathology
  • Glycine max / chemistry*
  • Humans
  • In Situ Nick-End Labeling
  • Isoflavones / pharmacology*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • RNA, Messenger / drug effects
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Time Factors
  • bcl-2-Associated X Protein

Substances

  • BAX protein, human
  • Isoflavones
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • bcl-2-Associated X Protein