The anti-sense RNA of HDAC1 induced the inhibition of proliferation and cell cycle arrest in MCF-7 cells, suggesting it might have therapeutic applications as an antitumor agent in breast cancer. Introduction Histone acetyltransferases (HATs) and histone deacetylases

acetylation and deacetylation are the main posttranslational modifications of histones. Increased deacetylation is associated with carcinogenesis, but the individual histone deacetylase (HDAC) responsible for this increase remains elusive. This study was designed to investigate the role of histone deacetylase 1 during tumorigenesis in McF-7 human breast cancer cells. Anti-sense RNA was used to downregulate HDAC1 expression. RT-PCR analysis confirmed the efficiency of the anti-sense RNA, revealing that anti-sense RNA effectively downregulated HDAC1. The MTT assay showed that the proliferation of MCF-7 cells was inhibited and that cell activity was decreased. Cell cycle analysis identified cell cycle phase variations, with cells mainly arrested in the G1 and G2 phase. The anti-sense RNA of HDAC1 induced the inhibition of proliferation and cell cycle arrest in MCF-7 cells, suggesting it might have therapeutic applications as an antitumor agent in breast cancer.