CHPF Affects Proliferation And Apoptosis Of Non-small Cell Lung Cancer By Activating MAPK Signaling Pathway

Background and purposeNon-small cell lung cancer(NSCLC)is the most malignant tumor with the highest morbidity and mortality.Recent studies have shown that chondroitin polymerization factor(CHPF)is abnormally expressed in some malignant tumors.However,the expression of CHPF in NSCLC has not been reported.In this study,we will explored the relationship between CHPF and NSCLC.MethodsFirst,differential genes present in NSCLC were screened by bioinformatics analysis.The expression status of CHPF in NSCLC tissues and cell lines were deteced by immunohistochemistry or Western blot,and the relationship between CHPF and prognosis of LUAD patients was analyzed.CHPF was effectively silenced in NSCLC 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 NSCLC tumor models.Western blot assay was performed to assess the expression changes of MAPK signaling pathway.ResultWe found that CHPF is highly expressed in NSCLC tissues and cell lines.In vitro experiments,CHPF knockdown in NSCLC cells is effective in inhibiting the proliferation of cancer cells and promoting their apoptosis.In in vivo experiments,CHPF knockdown significantly inhibited tumor growth in a xenograft model of NSCLC.ConclusionIt is worth noting that CHPF can also promote tumor progression by regulating the MAPK pathway.CHPF can promote the proliferation and anti-apoptosis of NSCLC cells,which is expected to be a potential target for NSCLC treatment.