GIT1 and neoplasm: In non-small-cell lung cancer (NSCLC) cells, miR-138 overexpression significantly suppressed cell growth and reversed EMT by targeting GIT1 and Sema4C, whereas silencing GIT1 and Sema4C by siRNA suppressed tumor cell proliferation and reversed EMT, which indicated that the inhibitory effects of miR-138 were partly rescued by abnormal GIT1 and Sema4C expression19.