In basal-type breast cancer, depletion of HDAC5 by shRNA not only hinders cell proliferation, manifesting as arresting G1 cell cycle, but also attenuates migration and colony formation of breast cancer cells through regulating LSD1 protein stability by decreasing LSD1 protein acetylation.34 Studies have also shown that deacetylase activity of HDAC5 is required for HIF-1α nuclear accumulation.35 In the present study, we found that HDAC5 is indispensable for SOX9 deacetylation. This evidence concerns the gene HIF1A and breast carcinoma.