Assessment of the Anticancer Effect of Chlorojanerin Isolated from Centaurothamnus maximus on A549 Lung Cancer Cells

The goal of this study was to assess the anticancer efficacy of chlorojanerin against various cancer cells. The effects of chlorojanerin on cell cytotoxicity, cell cycle arrest, and cell apoptosis were examined using MTT assay, propidium iodide staining, and FITC Annexin V assay. RT-PCR was employed to determine the expression levels of apoptosis-related genes. Furthermore, docking simulations were utilized to further elucidate the binding preferences of chlorojanerin with Bcl-2. According to MTT assay, chlorojanerin inhibited the proliferation of all tested cells in a dose-dependent manner with a promising effect against A549 lung cancer cells with an IC50 of 10 mu M. Cell growth inhibition by chlorojanerin was linked with G2/M phase cell cycle arrest in A549 treated cells. Flow cytometry analysis indicated that the proliferation inhibition effect of chlorojanerin was associated with apoptosis induction in A549 cells. Remarkably, chlorojanerin altered the expression of many genes involved in apoptosis initiation. Moreover, we determined that chlorojanerin fit into the active site of Bcl-2 according to the molecular docking study. Collectively, our results demonstrate that chlorojanerin mediated an anticancer effect involving cell cycle arrest and apoptotic cell death and, therefore, could potentially serve as a therapeutic agent in lung cancer treatment.

Automated summary

The aim of this study was to evaluate the anticancer efficacy of chlorojanerin against different cancer cells. The effects of chlorojanerin on cell cytotoxicity, cell cycle arrest, and cell apoptosis were investigated using various assays. RT-PCR was used to analyze the expression levels of apoptosis-related genes. Docking simulations were employed to study the binding preferences of chlorojanerin with Bcl-2. The results showed that chlorojanerin inhibited cell proliferation dose-dependently and had a promising effect against A549 lung cancer cells. The inhibition of cell growth was associated with G2/M phase cell cycle arrest and apoptosis induction. We also found that chlorojanerin altered the expression of genes involved in apoptosis initiation and could fit into the active site of Bcl-2 according to docking simulations. These findings suggest that chlorojanerin has potential as a therapeutic agent in lung cancer treatment.