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Article

Roburic Acid as a Therapeutic Candidate: Antiproliferative Activity and Secondary Cell Death Response in Colorectal Cancer Cells

1
Department of Molecular Biotechnology and Genetics, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland
2
Doctoral School of Exact and Natural Sciences, University of Lodz, Banacha Street 12/16, 90-237 Lodz, Poland
3
Laboratory of Microscopic Imaging and Specialized Biological Techniques, University of Lodz, Banacha Street 12/16, 90-237 Lodz, Poland
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2026, 27(5), 2478; https://doi.org/10.3390/ijms27052478
Submission received: 9 February 2026 / Revised: 4 March 2026 / Accepted: 6 March 2026 / Published: 8 March 2026

Abstract

Natural compounds are increasingly recognized as valuable sources of pharmacologically active agents for cancer therapy. Among them, plant-derived triterpenoids attract attention due to their structural diversity and broad biological activity. Roburic acid (RA), a tetracyclic triterpenoid, has previously been shown to exert antiproliferative effects in colorectal cancer (CRC) cells with limited cytotoxicity. In the present study, we investigated the cellular mechanisms underlying RA activity in CRC cells, focusing on cell cycle regulation, mitochondrial function, apoptosis, oxidative stress, and DNA integrity. RA treatment markedly suppressed CRC cell proliferation, resulting in G0/G1 cell cycle arrest and downregulation of key proliferation markers. Mitochondrial analysis revealed an early reduction in mitochondrial membrane potential (MMP) following RA exposure, indicating mitochondrial dysfunction. Importantly, these effects occurred in the absence of intracellular reactive oxygen species (ROS) generation and without induction of DNA strand breaks, demonstrating a non-pro-oxidant and non-genotoxic profile of RA. Apoptotic features were observed mainly at higher concentrations and after prolonged exposure and were strongly dependent on cell line and assay type. Overall, RA limits CRC cell growth predominantly through cytostatic mechanisms, including cell cycle arrest and mitochondrial modulation, while apoptosis is a secondary, context-dependent response. The lack of oxidative stress and genotoxicity distinguishes RA from many conventional cytotoxic agents and supports its further investigation as a non-genotoxic anticancer compound.
Keywords: roburic acid; colorectal cancer; cytostatic activity; cell cycle arrest; mitochondrial dysfunction; anti-proliferative activity roburic acid; colorectal cancer; cytostatic activity; cell cycle arrest; mitochondrial dysfunction; anti-proliferative activity

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MDPI and ACS Style

Gielecińska, A.; Kciuk, M.; Gruszka, R.; Wawrocki, S.; Kontek, R. Roburic Acid as a Therapeutic Candidate: Antiproliferative Activity and Secondary Cell Death Response in Colorectal Cancer Cells. Int. J. Mol. Sci. 2026, 27, 2478. https://doi.org/10.3390/ijms27052478

AMA Style

Gielecińska A, Kciuk M, Gruszka R, Wawrocki S, Kontek R. Roburic Acid as a Therapeutic Candidate: Antiproliferative Activity and Secondary Cell Death Response in Colorectal Cancer Cells. International Journal of Molecular Sciences. 2026; 27(5):2478. https://doi.org/10.3390/ijms27052478

Chicago/Turabian Style

Gielecińska, Adrianna, Mateusz Kciuk, Renata Gruszka, Sebastian Wawrocki, and Renata Kontek. 2026. "Roburic Acid as a Therapeutic Candidate: Antiproliferative Activity and Secondary Cell Death Response in Colorectal Cancer Cells" International Journal of Molecular Sciences 27, no. 5: 2478. https://doi.org/10.3390/ijms27052478

APA Style

Gielecińska, A., Kciuk, M., Gruszka, R., Wawrocki, S., & Kontek, R. (2026). Roburic Acid as a Therapeutic Candidate: Antiproliferative Activity and Secondary Cell Death Response in Colorectal Cancer Cells. International Journal of Molecular Sciences, 27(5), 2478. https://doi.org/10.3390/ijms27052478

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