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Peer-reviewedCC BY-NC 4.0Asian Pacific Journal of Cancer Prevention : APJCP

Sesamin Suppresses Ovarian Cancer Progression via Modulation of Wnt/β-Catenin and Associated Oncogenic Pathways

  • Heera Maheswari Jayaveeran1
  • Ponnulakshmi Rajagopal1
  • Manju Parthiban1
  • Selvaraj Jayaraman2
  • Sureka Varalakshmi V3
  • Krithika Chandrasekaran3
  1. 1Central Research Laboratory, Meenakshi Ammal Dental College, Meenakshi Academy of Higher Education and Research, Deemed to be University, Chennai-600095, India.
  2. 2Centre of Molecular Medicine and Diagnostics (COMManD), Department of Biochemistry, Saveetha Dental College & Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai-600077, India.
  3. 3Meenakshi Academy of Higher Education and Research, Deemed to be University. West K. K. Nagar, Chennai - 600078, Tamil Nadu, India.
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Abstract

Objective:: The current research aimed to explore the molecular pathway of sesamin in controlling the Wnt/β-catenin signaling pathway and associated oncogenic regulators in ovarian cancer cells.

Methods:: Molecular docking was conducted to assess sesamin’s binding activity toward major signaling proteins (Wnt, β-catenin, GSK3β, TGF-β). Functional confirmation was performed using quantitative PCR (qPCR) to quantify gene expression following a 48-hour treatment of ovarian cancer cells with sesamin.

Result:: Docking simulations revealed strong binding affinities, particularly with Wnt (−9.19 kcal/mol), supported by hydrogen bond interactions. qPCR results showed significant downregulation of Wnt (50%), TGF-β (40%), GSK3β (25%), and β-catenin transcripts compared to the control (p < 0.001).

Conclusion:: Sesamin potently inhibits several oncogenic regulators within the Wnt/β-catenin pathway, positioning it as a potential multi-target natural therapeutic for ovarian cancer. These findings support sesamin as a promising candidate for further preclinical and clinical investigation, particularly as an adjuvant therapy to overcome drug resistance and limit tumor progression.

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Cite

BibTeXRIS
BibTeX
@article{jayaveeran2026sesamin,
  title = {{Sesamin Suppresses Ovarian Cancer Progression via Modulation of Wnt/β-Catenin and Associated Oncogenic Pathways}},
  author = {Heera Maheswari Jayaveeran and Ponnulakshmi Rajagopal and Manju Parthiban and Selvaraj Jayaraman and Sureka Varalakshmi V and Krithika Chandrasekaran},
  journal = {Asian Pacific Journal of Cancer Prevention : APJCP},
  year = {2026},
  month = jun,
  doi = {10.31557/apjcp.2026.27.6.2149},
  url = {https://doi.org/10.31557/apjcp.2026.27.6.2149},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Sesamin Suppresses Ovarian Cancer Progression via Modulation of Wnt/β-Catenin and Associated Oncogenic Pathways
AU  - Heera Maheswari Jayaveeran
AU  - Ponnulakshmi Rajagopal
AU  - Manju Parthiban
AU  - Selvaraj Jayaraman
AU  - Sureka Varalakshmi V
AU  - Krithika Chandrasekaran
PY  - 2026
DA  - 2026/06/19
JO  - Asian Pacific Journal of Cancer Prevention : APJCP
DO  - 10.31557/apjcp.2026.27.6.2149
UR  - https://doi.org/10.31557/apjcp.2026.27.6.2149
AB  - Objective:: The current research aimed to explore the molecular pathway of sesamin in controlling the Wnt/β-catenin signaling pathway and associated oncogenic regulators in ovarian cancer cells.  Methods:: Molecular docking was conducted to assess sesamin’s binding activity toward major signaling proteins (Wnt, β-catenin, GSK3β, TGF-β). Functional confirmation was performed using quantitative PCR (qPCR) to quantify gene expression following a 48-hour treatment of ovarian cancer cells with sesamin.  Result:: Docking simulations revealed strong binding affinities, particularly with Wnt (−9.19 kcal/mol), supported by hydrogen bond interactions. qPCR results showed significant downregulation of Wnt (50%), TGF-β (40%), GSK3β (25%), and β-catenin transcripts compared to the control (p < 0.001).  Conclusion:: Sesamin potently inhibits several oncogenic regulators within the Wnt/β-catenin pathway, positioning it as a potential multi-target natural therapeutic for ovarian cancer. These findings support sesamin as a promising candidate for further preclinical and clinical investigation, particularly as an adjuvant therapy to overcome drug resistance and limit tumor progression.
SN  - 1513-7368
SN  - 2476-762X
ER  -