Anti- Cancer Potential of Diosgenin, a Steroidal Saponin, against Human Oral Cancer Cells

Dutta, Uma; Dey, Sonali; Boruah, Monikongkona; Sailo, Bethsebie Lalduhsaki; Muchahary, Bhaigyaroti; Kunnumakkara, Ajaikumar B

doi:10.31557/APJCP.2025.26.6.2049

Anti- Cancer Potential of Diosgenin, a Steroidal Saponin, against Human Oral Cancer Cells

Document Type : Research Articles

Authors

¹ Cell and Molecular Biology, Toxicology Laboratory, Department of Zoology, Cotton University, Guwahati, Assam, India.

² Department of Pathology, All India Institute of Medical Sciences, New Delhi, India.

³ Department of Biosciences and Bioengineering, Indian Institute of Technology, Guwahati, Assam, India.

10.31557/APJCP.2025.26.6.2049

Abstract

Objective: Oral squamous cell carcinoma (OSCC), affecting the lip and oral cavity, is one of the most prevalent cancers worldwide with the highest morbidity rate in the North-Eastern region of India. The current treatment options including surgery and chemotherapy are plagued by adverse side-effects and emergence of chemo-resistance, particularly against drugs like cisplatin and 5-fluorouracil. The present study focuses on demonstrating the effects of diosgenin, a naturally occurring steroidal saponin, on the survival, proliferation, and migration of OSCC cells in vitro. Methods: Preliminary in vitro screening of diosgenin in OSCC cells was performed using MTT, colony formation, cell cycle arrest, PI-FACS, live/dead, and wound-healing assays. In addition, the potential of diosgenin in regulating the expression of critical proteins involved in OSCC was evaluated using western blot analysis. Result: The present study shows that diosgenin exhibited selective anti-proliferative activity on OSCC cell lines SAS and HSC3 compared to normal kidney cell line HEK-293T. In addition, it enhances the chemosensitivity of SAS cells to cisplatin and 5-FU. This compound also displayed anti-clonogenic, cell cycle arrest, cytotoxic, and anti-migratory effects on SAS cells in a dose-dependent manner. Further, diosgenin regulated the expressions of COX-2, CXCR-4, VEGF, TWIST-1, p-AKT, and AKT, which are critical proteins for the development and progression of OSCC. Conclusion: These findings support the therapeutic potential of diosgenin, thereby opening a new avenue for oral cancer therapy. Nonetheless, the data needs to be further validated in in vivo and clinical settings.

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