Abstract:
:AR-42 is a member of a novelly discovered class of phenylbutyrate-derived histone deacetylase inhibitors, and has a number of antitumor effects in a variety of tumor types; however, the role of AR-42 and its possible mechanisms have not been reported in the treatment of breast cancer. The aim of the present study was to investigate the antitumor effects of AR-42 and its associated mechanisms in breast cancer. MTT assays and colony formation assays were conducted to measure the proliferation of MCF-7 cells, and flow cytometry was used to analyze cell apoptosis. The results revealed that AR-42 induced cell apoptosis and suppressed cell growth in a dose- and time-dependent manner. Mechanistically, AR-42 treatment increased the acetylation of the p53 protein and prolonged the half-life of the p53 protein; furthermore, AR-42 treatment upregulated p21 and PUMA expression. Notably, AR-42 had a synergistic effect on MCF-7 cells in combination with fluorouracil, which is one of the most commonly used chemotherapeutic agents. In conclusion, the results indicated that AR-42 inhibits breast cancer cell proliferation and induces apoptosis, indicating that AR-42 is a potential therapeutic agent.
journal_name
Oncol Lettjournal_title
Oncology lettersauthors
Zhou R,Wu J,Tang X,Wei X,Ju C,Zhang F,Sun J,Shuai D,Zhang Z,Liu Q,Lv XBdoi
10.3892/ol.2018.8854subject
Has Abstractpub_date
2018-08-01 00:00:00pages
1967-1974issue
2eissn
1792-1074issn
1792-1082pii
OL-0-0-8854journal_volume
16pub_type
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