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Genistein Suppresses v-Src-Driven Proliferative Activity by Arresting the Cell-Cycle at G2/M through Increasing p21

Misaki Ono1, Mikako Takeshima1, Asuka Nishi1

  • 1Graduate School of Health and Nutritional Sciences, Nakamura Gakuen University, Fukuoka, Japan.

Nutrition and Cancer
|July 25, 2020
PubMed

Insights

Genistein, a soy isoflavone, may suppress cancer cell growth driven by activated Src (a cancer-promoting protein). It uniquely halts cancer cells at G2/M phase, unlike other isoflavones, suggesting potential cancer prevention benefits.

Area of Science:

  • Oncology
  • Molecular Biology
  • Nutritional Science

Background:

  • Activated Src is implicated in human cancer development, progression, and metastasis.
  • Soy isoflavones show potential anticancer activity, but their effect on Src oncogenic activity is unknown.

Purpose of the Study:

  • Investigate the role of Src in the anti-proliferative activity of soy isoflavones (genistein, daidzein, glycitein, equol).
  • Determine if Src activation influences cellular response to these isoflavones.

Main Methods:

  • Utilized v-src-transfected human adenocarcinoma cells (HAG/src3-1) and control cells (HAG/neo3-5).
  • Assessed isoflavone effects on cell proliferation, cell cycle progression, and protein expression (p53, p21, cyclin-CDK complexes).

Main Results:

  • Genistein and equol potently inhibited control cell growth; daidzein and glycitein had modest effects.
  • Src activation conferred resistance to daidzein, glycitein, and equol, but increased sensitivity to genistein.
  • Genistein arrested Src-activated cells at G2/M phase, increasing p53 and p21 levels.
  • No apoptosis was induced; other isoflavones did not cause cell cycle arrest.

Conclusions:

  • Genistein is the only isoflavone that may suppress Src-driven proliferation by inducing G2/M arrest via p21.
  • Genistein offers a mechanistic rationale for preventing cancers with activated Src.

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