CHPF promotes lung adenocarcinoma proliferation and anti-apoptosis via the MAPK pathway

Abstract

ObjectiveRecent studies have shown that Chondroitin polymerizing factor (CHPF) is abnormally expressed in malignant tumors, however, the expression of CHPF in lung adenocarcinoma (LUAD) has not been reported. In this study, the relationship of CHPF and LUAD will be explored. MethodsDifferential genes present in LUAD were screened by bioinformatics analysis. The expression status of CHPF in LUAD tissues and cell lines were deteced by Western blotting or Real-time Quantitative Polymerase Chain Reaction Detecting System (qPCR), and the relationship between CHPF and prognosis of LUAD patients was analyzed. CHPF was effectively silenced in LUAD cell lines by lentivirus- mediated methods. The effect of CHPF on proliferation, cell cycle progression and apoptosis of cancer cells was assessed. We further determined the role of CHPF in tumor growth in vivo by using xenograft LUAD tumor models. Western blotting assay was performed to assess the expression changes of MAPK signaling pathway. ResultsWe found that CHPF is highly expressed in LUAD tissues and cell lines. In vitro experiments, CHPF knockdown in LUAD cells can effectively inhibit proliferation and promote apoptosis of cancer cell. In vivo experiment, tumor growth was markedly inhibited by CHPF knockdown in the xenograft model of LUAD. Notably, CHPF also could promote tumor progression by regulating MAPK pathway. ConclusionCHPF can promote the proliferation and antiapoptosis of LUAD cells, which is promising to become a potential target for LUAD treatment.