Bisphenol A suppresses colon epithelial cell responses via G0/G1-phase arrest, MAPK and PI3K/AKT pathway modulation,

Jun-Hui Song1, Daeun Lee1, Byungdoo Hwang1

  • 1Department of Food and Nutrition, Chung-Ang University, 4726 Seodong-Daero, Daedeok-Myeon, Anseong, 17546, South Korea.

Scientific Reports
|July 22, 2025
PubMed

Insights

Bisphenol A (BPA) exposure harms human colonic cells by inhibiting their growth and movement. This endocrine disruptor impacts cell cycle and signaling pathways, with effects reversed by targeting p21WAF1.

Area of Science:

  • Toxicology
  • Cell Biology
  • Gastroenterology

Background:

  • Bisphenol A (BPA) is an endocrine-disrupting chemical found in plastics.
  • BPA exposure is linked to damage in reproductive, immune, and neuroendocrine systems.
  • Mechanisms of BPA's effects on the intestinal tract remain unclear.

Purpose of the Study:

  • To investigate the adverse effects of BPA on human colonic epithelial cells.
  • To elucidate the molecular mechanisms underlying BPA's impact on colonic cell proliferation, migration, and invasion.

Main Methods:

  • In vitro assays were performed on HCT 116 and HCT-8 human colonic epithelial cells.
  • Assays included viability, proliferation, invasion, and migration.
  • Cell cycle progression, MAPK/AKT pathways, and transcription factor binding were analyzed. p21WAF1 was silenced using siRNA.

Main Results:

  • BPA suppressed colonic cell proliferation by altering cell cycle progression and modulating MAPK/AKT pathways.
  • BPA inhibited matrix metalloproteinases-2 and -9 induction by interfering with transcription factors (SP-1, NF-κB, AP-1).
  • BPA-induced effects on proliferation, migration, invasion, and MAPK/AKT signaling were reversed by silencing p21WAF1.

Conclusions:

  • BPA inhibits human colonic epithelial cell proliferation and mobility.
  • The mechanism involves p21WAF1 induction, affecting cell cycle and signaling pathways.
  • This study clarifies BPA's detrimental effects on the colon at a cellular level.

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