Beta-sitosterol regulates PTGS1 to inhibit gastric cancer cell proliferation and angiogenesis

Jindao Wang1, Minghui Zhou2, Qiuli Zhou2

  • 1Department of Endoscopy Center, Shaoxing People's Hospital, Shaoxing 312000, China.

Abstract

Insights

Beta-sitosterol (BS) targets PTGS1 to inhibit gastric cancer (GC) cell proliferation and angiogenesis. This study identifies BS as a potential therapeutic agent for GC, offering new insights into its anti-cancer mechanisms.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Gastric cancer (GC) is a leading cause of cancer mortality worldwide.
  • Beta-sitosterol (BS), a phytosterol, exhibits anti-proliferative effects on tumors.
  • The precise mechanisms and molecular targets of BS in cancer remain largely unexplored.

Purpose of the Study:

  • To identify the molecular targets of beta-sitosterol (BS) in gastric cancer (GC) treatment.
  • To investigate the anti-cancer effects of BS on GC cells.
  • To validate the interaction between BS and its target protein.

Main Methods:

  • Network pharmacology was employed to predict BS targets in GC.
  • Molecular docking and cellular thermal shift assay (CETSA) were used to validate BS-PTGS1 binding.
  • In vitro assays (Cell Counting Kit-8, clone formation, flow cytometry, western blot) assessed BS effects on GC cell viability, proliferation, apoptosis, and angiogenesis.

Main Results:

  • PTGS1 was identified as a direct binding protein target of BS in GC cells.
  • BS demonstrated significant inhibition of GC cell proliferation and angiogenesis in vitro.
  • BS treatment counteracted the pro-proliferative and pro-angiogenic effects of PTGS1 overexpression in GC cells.

Conclusions:

  • PTGS1 is a key molecular target of beta-sitosterol (BS) in gastric cancer (GC) cells.
  • BS effectively inhibits GC cell proliferation and angiogenesis by regulating PTGS1.
  • These findings support the potential of BS as a therapeutic agent for gastric cancer.

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