# Coumestrol induces apoptosis and inhibits invasion in human liver cancer cells

## TL;DR

Coumestrol, a natural compound, shows promise in fighting liver cancer by killing cancer cells and preventing their spread.

## Contribution

This study is among the first to demonstrate coumestrol's anti-cancer effects on liver cancer cells through apoptosis and invasion inhibition.

## Key findings

- Coumestrol induced significant toxicity and apoptosis in HepG2 liver cancer cells.
- The compound inhibited cell invasion by suppressing MMP-2 and MMP-9 gene expression.
- Apoptosis was confirmed through caspase activation and Bax expression in treated cells.

## 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.