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  11. Pachymic Acid Promotes Ferroptosis And Inhibits Gastric Cancer Progression By Suppressing The Pdgfrb-mediated Pi3k/akt Pathway

Pachymic acid promotes ferroptosis and inhibits gastric cancer progression by suppressing the PDGFRB-mediated PI3K/Akt pathway

Jinlin Nie1,2, Haoran Zhang2, Xiaofeng Li1

  • 1Department of Hepatobiliary Pancreatic Hernia Surgery, The Affiliated Guangdong Second Provincial General Hospital of Jinan University, Guangzhou, 510317, People's Republic of China.

Heliyon
|November 8, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Pachymic acid (PA), a compound from Poria cocos, inhibits gastric cancer (GC) growth by inducing ferroptosis. It targets PDGFRB, altering the PI3K/Akt pathway, offering potential new therapies for gastric cancer.

Area of Science:

  • Oncology
  • Pharmacology
  • Traditional Chinese Medicine

Background:

  • Gastric cancer (GC) presents high global incidence and mortality, with persistent challenges in treatment efficacy, recurrence, and drug resistance.
  • Investigating novel therapeutic agents, particularly from traditional Chinese medicine, is crucial for developing effective anti-gastric cancer strategies.

Purpose of the Study:

  • To investigate the anti-gastric cancer effects of Pachymic acid (PA), a triterpenoid from Poria cocos.
  • To elucidate the underlying mechanisms, including ferroptosis induction and potential molecular targets, of PA's anti-tumor activity in GC.

Main Methods:

  • In vitro and in vivo experiments were conducted to assess PA's effects on GC cell proliferation, migration, and invasion.
  • Ferroptosis was evaluated using biochemical assays (malondialdehyde, Fe2+, ROS, glutathione).
Keywords:
FerroptosisGastric cancerPDGFRBPI3K/Akt signalling pathway

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  • High-throughput sequencing and TCGA database analysis identified PDGFRB as a potential target, with subsequent in vivo validation.

    • Main Results:

    • PA significantly inhibited proliferation, migration, and invasion of gastric cancer cells.
    • PA treatment induced ferroptosis in GC cells, evidenced by altered levels of key ferroptosis markers.
    • PDGFRB was identified as a downstream target of PA; its overexpression counteracted PA's anti-tumor effects.
    • The PI3K/Akt signaling pathway was implicated in PA-induced ferroptosis.

    Conclusions:

    • Pachymic acid exhibits anti-gastric cancer properties by inducing ferroptosis.
    • PA's mechanism involves targeting PDGFRB and modulating the PI3K/Akt signaling pathway.
    • PA represents a promising candidate for developing novel therapeutic strategies against gastric cancer.
    Pachymic acid