Coumestrol induces apoptosis and inhibits invasion in human liver cancer cells

Theodor Bilharz Research Institute

Bibliographic Information

Authors: Abdul-Nabie H.; Samir S.; Aboshousha T.; Fares N.; Abo-Zeid F.S.

Journal: Toxicology Reports

Publisher: Elsevier Inc.

Publication Date: December 2025

Volume / Issue: Volume 15

Article No.: 102091

ISSN: 22147500

DOI: 10.1016/j.toxrep.2025.102091

Scopus: View on Scopus

Document Type: Article

Access: All Open Access; Gold Open Access; Green Open Access

Authors and Affiliations

Abdul-Nabie H., Zoology Department, Faculty of Science, Ain Shams University, Egypt; Samir S., Biochemistry and Molecular Biology Department, Theodor Bilharz Research Institute, Giza, Egypt; Aboshousha T., Pathology Department, Theodor Bilharz Research Institute, Giza, Egypt; Fares N., Zoology Department, Faculty of Science, Ain Shams University, Egypt; Abo-Zeid F.S., Zoology Department, Faculty of Science, Ain Shams University, Egypt

Abstract

Hepatocellular carcinoma (HCC) is a major public health problem, with a poor prognosis in patients with advanced disease. We aimed to investigate the cytotoxic activity of coumestrol against human hepatocellular carcinoma HepG2 cells. Crystal violet (CV) assay was performed for cell cytotoxicity assessment on Vero cells (normal Kidney) and HepG2 cells. Apoptosis was analyzed by Annexin V/FITC staining. The relative expression of BAX, bcl-2, NF-Kβ, PCNA, MMP2, Caspase-3, Caspase-9, COX2, and MMP9 was detected using quantitative real-time PCR (qPCR). In addition, immunohistochemical analysis (IHC) of Bax, and PCNA were established. Results indicated that coumestrol induced significant toxicity in HepG2 cells. Annexin V-FITC staining assays revealed that coumestrol-induced cytotoxicity in HepG2 cells was mediated through apoptosis stimulation. The apoptosis in HepG2 cells was mediated through caspase-activation. Cell invasion was inhibited by coumestrol in HepG2 cells via inhibition of MMP-2 and MMP-9 expressions. IHC confirmed the strong expression of Bax and nuclear expression of PCNA in treated cells. To the best of our knowledge, limited studies have investigated the impact of coumestrol. The study showed that coumestrol exhibited cytotoxic and apoptotic effects against HepG2 cells, accompanied by inhibition of invasion-related gene expression. © 2025 The Authors

Keywords

Apoptosis; Coumestrol; Expression of genes; Immunohistochemistry; Liver cancer; Quantitative real-time PCR; caspase 3; caspase 9; cyclooxygenase 2 inhibitor; gelatinase A; gelatinase B; glyceraldehyde 3 phosphate dehydrogenase; immunoglobulin enhancer binding protein; protein Bax; protein bcl 2; xylene; animal cell; Article; cancer prognosis; cell invasion; cell proliferation; cell viability; centrifugation; chemical structure; colorimetry; controlled study; cytotoxicity; flow cytometry; gene expression; Hep-G2 cell line; histopathology; human; human cell; IC50; light microscopy; liver cancer cell line; liver cell carcinoma; nonhuman; protein expression; public health; real time polymerase chain reaction; Vero cell line

Citation Information

Scopus Citations: 0

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