Gallic acid inhibits bladder cancer cell proliferation and migration via regulating fatty acid synthase (FAS)

Chung-Chia Liao1, Shu-Chun Chen2, Hui-Pei Huang2,3,4

  • 1Division of Endocrinology and Metabolism, Department of Internal Medicine, Cheng-Ching Hospital, Taichung, Taiwan.

Insights

Gallic acid (GA) effectively inhibits bladder cancer cell growth and migration by targeting fatty acid synthase (FAS). This natural compound also regulates cell proliferation and invasion pathways, offering potential therapeutic benefits.

Area of Science:

  • Oncology
  • Biochemistry
  • Pharmacology

Background:

  • Bladder cancer ranks as the ninth most prevalent cancer globally.
  • Cytotoxic drugs have advanced bladder cancer treatment.
  • Gallic acid (GA) shows promise in inhibiting carcinogenesis.

Purpose of the Study:

  • To investigate the effects of Gallic acid (GA) on bladder cancer cell proliferation and migration.
  • To elucidate the molecular mechanisms underlying GA's anti-cancer activity.

Main Methods:

  • Assessing fatty acid synthase (FAS) activity and ER alpha levels in TSGH-8301 cells.
  • Analyzing cell proliferation via PI3K/AKT and MAPK/ERK pathways.
  • Utilizing immunoprecipitation assays to examine Skp2 and p27 interactions.
  • Employing transwell chambers assays to evaluate cell invasion and migration.

Main Results:

  • Gallic acid inhibited fatty acid synthase (FAS) activity and increased ER alpha levels.
  • GA regulated cell proliferation through PI3K/AKT and MAPK/ERK pathways.
  • GA decreased Skp2 protein levels, attenuated Skp2-p27 association, and inhibited G2/M phase transition.
  • GA suppressed bladder cancer cell invasion and migration via the p-AKT/MMP-2 signaling pathway.

Conclusions:

  • Gallic acid effectively inhibits the growth, invasion, and migration of TSGH-8301 bladder cancer cells.
  • Inhibition of fatty acid synthase (FAS) is a key mechanism for GA's anti-cancer effects.
  • GA demonstrates potential as a therapeutic agent for bladder cancer.

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