AIBP promotes cell proliferation and migration through MAPK/ERK1/2 signaling pathway in hepatocellular carcinoma

Abstract Background: Apolipoprotein A-I binding protein (AIBP) is the major apolipoprotein of high-density lipoproteins (HDLs), which plays an important role in cholesterol metabolism and angiogenesis, as well as a variety of inflammation-related diseases, including cancer. However, the roles of AIBP in hepatocellular carcinoma (HCC) remains unclear. Methods: The expression of AIBP and its relationship with clinical prognosis were analyzed based on The Cancer Genome Atlas (TCGA) database. Western blotting (Wb) and immunohistochemistry (IHC) were used to analyze the expression of AIBP in human HCC tissues. CCK-8 and Colony-formation assays were used to evaluate the abilities of cell proliferation in vitro. Transwell and wound-healing assays were used to assess cell migration and invasion rate. The xenograft tumor model was used to explore the proliferation ability of HCC cells in nude mice. Results: The expression levels of AIBP were significantly higher in HCC tissues than that in adjacent normal tissues. Patients with high AIBP expression showed poor prognosis. Overexpression of AIBP in SMMC-7721 cells could promote cell proliferation, migration and invasion. Conversely, knockdown of AIBP in HCC-LM3 cells significantly reduced cell proliferation, migration and invasion in vitro. In addition, overexpression of AIBP could promote the proliferation ability of HCC cell in vivo. Finally, we found that AIBP could regulate the expression of MAPK signaling pathway related gene, such as ERK1/2, P-ERK1/2, MEK, P-MEK and c-Myc, and GDC-0994, a specific inhibitor of ERK1/2, could attenuated cell proliferation and migration abilities induced by overexpression of ABIP. Conclusions: These results suggested that high expression of AIBP in HCC tissues may promote cell proliferation, migration and invasion through MAPK/ERK signaling pathway. AIBP was expected to be a potential marker for early diagnosis and prognosis of HCC.