Anti-cancer effects of carvacrol on NUF2, CASP3 and CLDN6 expression in T47D breast cancer cells.

Breast cancer (BC) remains a major global health challenge, with rising incidence and mortality despite advances in diagnosis and treatment. Identifying new therapeutic agents targeting key molecular pathways is critical for improving patient outcomes. This study investigated the anticancer potential of carvacrol, a natural monoterpenoid phenol, in T47D luminal A BC cells, focusing on its effects on cell viability, migration, oxidative stress, and the expression of NUF2, CASP3 and CLDN6. T47D cells were treated with 480 µM carvacrol for 48 h. Cell viability, wound healing assay, intracellular reactive oxygen species (ROS) levels assay and gene expression were evaluated. Carvacrol significantly inhibited cell viability and reduced wound closure compared with controls. It markedly decreased intracellular ROS levels, indicating modulation of cellular redox status. Gene expression analysis revealed a significant downregulation of NUF2 (P < 0.01) and upregulation of both CASP3 (P < 0.01) and CLDN6 (P < 0.001). These findings suggest that carvacrol treatment is associated with transcriptional changes in genes related to proliferation, apoptosis, and cell junction dynamics. Carvacrol exhibits anticancer-related effects in T47D luminal A BC cells by altering cell viability, migration, oxidative stress, and the expression of NUF2, CASP3, and CLDN6. While these results highlight carvacrol's multi-targeted transcriptional impact, further studies are required to clarify the underlying molecular mechanisms and functional consequences.