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Rac1 in gastric cancer: a molecular driver of invasion, EMT, and therapeutic resistance

Jianwen Li1, Yahong Zhu2,3, Ruifeng Duan1

  • 1Gastroenteric Medicine and Digestive Endoscopy Center, The Second Hospital of Jilin University, Changchun, Jilin, 130042, China.

Journal of Translational Medicine
|November 4, 2025
PubMed

Insights

Ras-related C3 botulinum toxin substrate 1 (Rac1) drives gastric cancer growth and metastasis. Targeting Rac1 with inhibitors or immunotherapy offers potential for advanced gastric cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Gastric cancer (GC) is a leading cause of cancer mortality globally.
  • Advanced GC requires novel therapeutic strategies like targeted therapy and immunotherapy.
  • Ras-related C3 botulinum toxin substrate 1 (Rac1) is implicated in cancer progression.

Purpose of the Study:

  • To review the role of Rac1 in gastric cancer development, invasion, and metastasis.
  • To explore Rac1's regulatory mechanisms and involvement with factors like hypoxia and H. pylori.
  • To summarize current and emerging therapeutic strategies targeting Rac1.

Main Methods:

  • Literature review of studies on Rac1 in gastric cancer.
  • Analysis of Rac1's signaling pathways and regulatory dynamics.
  • Summary of therapeutic interventions targeting Rac1, including inhibitors and immunotherapy.

Main Results:

  • Rac1 is a key driver of gastric cancer growth, epithelial-to-mesenchymal transition (EMT), and metastasis.
  • Factors like hypoxia, oxidative stress, and H. pylori infection influence Rac1 activity.
  • Small-molecule inhibitors, miRNAs, and immunotherapy show promise for targeting Rac1.

Conclusions:

  • Rac1 is a critical therapeutic target and potential biomarker for gastric cancer.
  • Further research into Rac1-targeting strategies can advance precision medicine for GC.
  • Understanding Rac1's role is crucial for developing effective treatments for advanced gastric cancer.
Keywords:
Gastric cancerImmunotherapyMolecular inhibitorsRac1Rho GTPasesSignaling pathwaysmiRNA

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