miR‐483‐3p suppresses the proliferation and progression of human triple negative breast cancer cells by targeting the HDAC8>oncogene

Triple negative breast cancer (TNBC) is a heterogeneous subclass of breast cancer (BC) distinguished by lack of hormone receptor expression. It is highly aggressive and difficult to treat with traditional chemotherapeutic regimens. Targeted‐therapy using microRNAs (miR) has recently been proposed to improve the treatment of TNBC in the early stages. Here, we explore the roles of miR‐483‐3p/HDAC8 HDAC8 premiR‐vector on tumorigenicity in TNBC patients. Clinical TNBC specimens and three BC cell lines were prepared. miR‐483‐3p and expression levels were measured using quantitative real‐time polymerase chain reaction. Cell cycle progression was assessed by a flow‐cytometry method. We also investigated cell proliferation by 3‐2, 5‐diphenyl tetrazolium bromide assay and colony formation assay. We used a to overexpress miR‐483‐3p, and a HDAC8‐KO‐vector for knocking out the endogenous production of HDAC8. Our data showed significant downregulation of miR‐483‐3p expression in TNBC clinical and cell line samples. The HDAC8 was also upregulated in both tissue specimens and BC cell lines. We found that increased levels of endogenous miR‐483‐3p affects tumorigenecity of MDA‐MB‐231. Downregulation of HDAC8 using the KO‐vector showed the same pattern. Our results revealed that the miR‐483‐3p suppresses cellular proliferation and progression in TNBC cell lines via targeting HDAC8. Overall, our outcomes demonstrated the role of miR‐483‐3p as a tumor suppressor in TNBC and showed the possible mechanism via HDAC8. In addition, targeted treatment of TNBC with miR‐483‐3p might be considered in the future. HDAC8 is overexpressed in triple negative breast cancer (TNBC). miR‐483‐3p is downregulated in TNBC. Upregulation of miR‐483‐3p expression can reverse oncogenic function of HDAC8 by direct targeting of its 3′‐untranslated region (3′‐UTR).