Blumea balsamifera Extract Induces Apoptosis and Cell Cycle Arrest in T47D Cell Line

Blumea balsamifera L. has demonstrated anti-cancer activity in various cancer cell types; however, its effectiveness against breast cancer remains underexplored. This study aimed to evaluate the anti-breast cancer activity of the ethanolic extract of B. balsamifera leaves (BEE) on T47D breast cancer cells. Cytotoxicity was assessed to determine the half-maximal inhibitory concentration (IC₅₀), followed by apoptosis and cell cycle analysis. Molecular simulations were conducted to explore potential mechanisms of BEE toxicity. BEE showed moderate cytotoxicity toward T47D cells, with an IC₅₀ of 72 µg/mL. The extract decreased cell viability by inducing apoptosis in a dose-dependent manner and caused cell cycle arrest at sub-G1 and S phases. Molecular docking revealed that compounds such as blumeatin, luteolin-7-methyl ether, quercetin, rhamnetin, and taxifolin 4′-methyl ether had stronger binding affinities to cyclin-dependent kinase 4 (CDK-4) than the reference drug abemaciclib. These compounds formed diverse interactions with CDK-4, predominantly via hydrogen bonds and π interactions. Molecular dynamics simulations further confirmed the stability of these compound–CDK-4 complexes. In summary, BEE exhibits cytotoxic effects on breast cancer cells through apoptosis induction, cell cycle arrest, and CDK-4 inhibition. These findings highlight its potential as a therapeutic candidate for hormone receptor–positive breast cancer, particularly the luminal A subtype.