sodium butyrate as histone deacetylase inhibitor can alter mir-101, zeb1, zeb2, and e-cadherin expression in mda-mb-468 cells as triple negative breast cancer cells

Background: triple-negative breast cancer (tnbc) is the most aggressive breast cancer subtype in women worldwide. the various alterations in the expression of different micrornas (mirnas) have been reported as crucial in the development of metastasis in breast tumors. objectives: this study investigated the effect of sodium butyrate (nab) on cell survival, cell metastasis and expression of mir-101, zeb1, zeb2 and e- cadherin in mda-mb-468 cells as a tnbc cell line. methods: cell viability was evaluated using the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (mtt assay), and the metastasis potential of mda-mb-468 cells was investigated using the scratch and transwell assay. the expression of genes involved in the metastasis process was measured using real-time polymerase chain reaction (pcr). results: the mtt assay showed that nab attenuated mda-mb-468 cell survival dose-dependently with an ic 50 value of 3.1 mm after 72 h treatment. the scratch and transwell assays also showed the anti-metastatic potential of nab. the expression of mir-101, e-cadherin, zeb1, and zeb2 was significantly difference in mda-mb-468 cells treated with 3.1 mm nab after 72 hours (p < 0.05). e-cadherin and mir-101 were up-regulated, while the expression of zeb1 and zeb2 was significantly down-regulated compared to the untreated cells. this suggests that nab increased cell attachment and prevented metastasis. in addition, nab (ic 50 value) restored the expression of mir-101, as a tumor suppressor, in mda-mb-468 cells confirming its anti-cancer potency. conclusions: sodium butyrate can be used as a drug to suppress invasion and cell migration in tnbc cells. however, further studies are needed to demonstrate the putative anti-metastatic mechanism of nab in preclinical and clinical settings.