Abstract

In breast carcinoma, epigenetic modifications, particularly disruption of histone acetylation, have become a significant research focus in recent years for discovering new treatments. Tannic acid (TA) has emerged as one of the promising anti-cancer polyphenolic compounds that suppresses the growth of cancer cells via the suppression of major stages of carcinogenesis. TA is not only a potent inhibitors of the hallmarks of cancer but also it provides pharmacological scaffolds that modulate the epigenetic regulation of gene expression. We investigated in vitro antiproliferative and epigenetic impacts of TA on MCF-7 human breast cancer cells. To our knowledge, there is no preclinical research investigating the epigenetic effect of TA on breast cancer by assessing histone deacetylases (HDACs) expression. The MCF-7 cell viability after TA treatment (12.5-200 μM) for 24-hours was assessed by the MTT assay. To determine the HDACs gene expression changes, total RNA was isolated from MCF-7 cells treated with TA and untreated control cells. The cDNAs were synthesized by Reverse transcription assay and gene expressions were analyzed using qRT-PCR. We found that TA can suppress MCF-7 cell proliferation with a dose-dependent manner as the IC50 was 103.7 μM for 24 h. Also, TA treatment led to a marked downregulation of HDAC1, HDAC2, HDAC3, and HDAC4 expression in MCF-7 cells. This downregulation suggesting that TA may suppress breast cancer cell growth by modulating histone deacetylases activity and potentially inducing epigenetic changes.

Key words: Breast cancer, histone deacetylases, histone deacetylases inhibitors, tannic acid