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A Di-Rhamnolipid (Rha2-C10-C10) Inhibits Colorectal Cancer Motility and Immune Evasion Through AKT-Associated

Sultan Pulat1, Prima F Hillman2, Jaeyoung Ko3

  • 1College of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Jeonnam, Republic of Korea.

Biofactors (Oxford, England)
|July 8, 2026
PubMed

Insights

This study shows that Rha2-C10-C10, a natural compound, effectively reduces colorectal cancer (CRC) cell movement, metabolism, and immune evasion. It targets key pathways involved in tumor progression, offering potential for CRC treatment.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Colorectal cancer (CRC) progression relies on metastasis, metabolic changes, and immune evasion.
  • Natural compounds are explored for their potential in cancer therapy.

Purpose of the Study:

  • To investigate the effects of the di-rhamnolipid Rha2-C10-C10 on CRC cell motility, metabolism, and immune signaling.
  • To assess the therapeutic potential of Rha2-C10-C10 against CRC.

Main Methods:

  • Assessed cytotoxicity of Rha2-C10-C10 in various CRC cell lines.
  • Evaluated effects on cell invasion, migration, and expression of key markers (e.g., N-cadherin, Snail, Slug, MMPs, TIMP2).
  • Analyzed impact on metabolic regulators (GLUT1, LDHA, HK2) and immune evasion factors (PD-L1, IDO1, IDO2, Galectin).
  • Investigated mechanisms involving AKT signaling pathways.

Main Results:

  • Rha2-C10-C10 suppressed CRC cell invasion and migration, particularly in Caco2 cells.
  • Downregulation of mesenchymal markers and matrix metalloproteinases, with increased TIMP2 expression observed.
  • Attenuated metabolic activity by reducing glycolytic regulators.
  • Suppressed immune evasion factors like PD-L1 and IDO.
  • Mechanisms involve modulation of AKT signaling.

Conclusions:

  • Rha2-C10-C10 effectively inhibits colorectal cancer cell motility, metabolic activity, and immune evasion.
  • Compound 1 demonstrates potential as a natural therapeutic agent targeting multiple CRC-promoting processes.
  • Further research into Rha2-C10-C10 is warranted for CRC treatment development.
Keywords:
AKTPD‐L1glycolysisimmune evasionmetastasisrhamnolipids

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