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Oncogenic microRNA‐765 promotes the growth and metastasis of breast carcinoma by directly targeting ING4

Previous investigations have proved that microRNA (miR)‐765 is significantly overexpressed in multiple tumor types. Nevertheless, the underlying molecular mechanism of miR‐765 in mediating breast carcinoma cell growth and metastasis remains unclear. Quantitative real‐time polymerase chain reaction was used to determine the levels of miR‐765 and inhibitor of growth 4 (ING4) in breast carcinoma tissues and breast carcinoma cells. Cell proliferation, colony formation, wound healing, and Transwell invasion assays were used to analysis the role of miR‐765 on breast carcinoma cell growth and aggressiveness. The expressions of ING4 were determined using Western blot analysis and immunohistochemical staining. The direct target of ING4 and miR‐765 was confirmed using the luciferase reporter assay. Nude mice were subcutaneously implanted with miR‐765 inhibitor transfected MDA‐MB‐231 cells to determine the potential role of miR‐765 in tumor growth in vivo. We observed that miR‐765 is overexpressed in breast carcinoma tissue and breast cancer cells. By using luciferase reporter gene bioassay, we find that ING4 is the direct target of miR‐765 in breast carcinoma. The level of ING4 is inversely associated with the level of miR‐765. The gain‐of‐function and loss‐of‐function experiments in vitro indicate that the downregulation of miR‐765 suppresses the growth, mobility, and invasion abilities of breast cancer cells by inhibiting ING4. In addition, overexpression of ING4 suppresses the aggressiveness of the MDA‐BA‐231 cell that is induced by miR‐761 in vitro. In this study, we prove that miR‐765 regulates the growth and metastasis of breast cancer via modulating miR‐765‐ING4‐negative feedback loop.