APLN 及其受体在肝细胞癌中的表达及其临床意义.

Objective To elucidate the expression of Apelin (APLN) and APLN receptor (APLNR) in hepatocellular carcinoma (HCC) and its potential mechanism affecting the occurrence and development of HCC. Methods UALCAN and GEPIA websites were used to analyze the expression of APLN and APLNR in HCC and their effects on survival rate. Then TIMER website and STRING database were used to analyze the possible molecular mechanism of APLN promoting the occurrence and development of HCC. Results Com- pared with normal samples, the transcription level of APLN in HCC was significantly up-regulated, and the transcription level of APLNR was not significantly changed. The survival of HCC patients with high APLN expression was significantly shortened, and there was no significant correlation between APLNR expression level and survival prognosis of HCC patients. The abnormal expression of APLN was positively correlated with vascular endothelial growth factor A(VEGFA). Hypoxia inducer factor 1, FMS-related tyrosine kinase 1, neurociliin 2 and VEGFR2 all interact with APLN-VEGFA, and were mainly involved in regulating endothelial cell proliferation and angiogenesis. Conclusion APLN is significantly highly expressed in HCC and is not conducive to the survival and prognosis of patients. APLN may promote the occurrence and development of HCC by regulating VEGFA to promote the proliferation and angiogenesis of tumor vascular endothelial cells, suggesting that APLN is a new potential diagnostic marker and therapeutic target for HCC. [ABSTRACT FROM AUTHOR]