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Updated: Jul 10, 2026
08:12
Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans
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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
Summary
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.
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