SELECTIVE CYTOTOXICITY AND APOPTOSIS INDUCTION BY SAHA IN MCF-7 CELL LINE
Abstract
Specific cytotoxicity against MCF-7 BC cells is shown by SAHA, which causes dose- and time-dependent declines in the cells' viability levels, with IC₅₀ values decreasing from 6 µM at 24 hours to 2 µM at 72 hours. In contrast, WI-38 normal fibroblasts demonstrate higher IC₅₀ values and reduced sensitivity, indicating minimal impact on normal cells. SAHA treatment leads to G₂/M phase cell cycle arrest and promotes apoptosis in MCF-7 cells, accompanied by upregulation of p21 and downregulation of MMP-9, suggesting inhibition of proliferation and metastatic potential. These findings support SAHA's potential as a targeted epigenetic therapeutic agent for BC.
These findings suggest that SAHA selectively inhibits proliferation and induces apoptosis in MCF-7 breast cancer cells through mechanisms involving G2/M cell cycle arrest and modulation of apoptosis-related genes, while sparing normal fibroblasts, highlighting its potential as a targeted epigenetic therapy for BC treatment.
Author contribution
OH: conducted the experimental work, MM, GN, WSA: conceptualized the idea and supervised the work, GN: wrote the MS.
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