Objective To evaluate the correlation between programmed death-ligand 1(PD-L1)expression in primary lung cancer cells,tumor associated macrophages(TAM)and patients’clinicopathological characteristics.Methods From 200...Objective To evaluate the correlation between programmed death-ligand 1(PD-L1)expression in primary lung cancer cells,tumor associated macrophages(TAM)and patients’clinicopathological characteristics.Methods From 2008 to 2010,208 non-small cell lung cancer patients who underwent surgery or CT-guided biopsy were recruited from Huadong Hospital,Fudan University.Immunohistochemistry staining was performed to evaluate the PD-L1 expression in both primary lung cancer cells and CD68 positive TAM.The relationship between PD-L1 expression and the clinical pathology was evaluated usingχ2test.Spearman’s rank correlations were used to determine the correlation between PD-L1 expression in tumor cells and macrophages.Results Positive PD-L1 expression in primary cancer cells was found in 136(65.3%)patients,which were negatively correlated with lymph node metastasis(P=0.009)and smoking history(P=0.036).Besides,TAM with PD-L1 expression(found in 116 patients)was positively associated with smoking history(P=0.034),well-differentiation(P=0.029)and negative lymph node metastasis(P=0.0096).A correlation between PD-L1 expression in primary tumor cells and non-small cell lung cancer associated macrophages was found(r=0.228,P=0.021).Conclusion PD-L1,secreted from TAM,might induce cancer cells apoptosis,and decrease lymph node metastasis.展开更多
Background:Apelin,an endogenous ligand of G-protein coupled receptor(GPCR),is a secreted peptide involved in the development of various tumors.However,the relationship between apelin and non-small cell lung cancer(NSC...Background:Apelin,an endogenous ligand of G-protein coupled receptor(GPCR),is a secreted peptide involved in the development of various tumors.However,the relationship between apelin and non-small cell lung cancer(NSCLC)is not quite clear.This study was designed to investigate the effect and mechanism of apelin on cell proliferation,migration and invasion of NSCLC cells.Methods:Twelve NSCLC specimens were collected for hematoxylin-eosin(HE)staining and immunohistochemistry analyses.Cell proliferation was examined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)and cell migration and invasion were assessed using wound-healing and transwell assays.The subcellular location of yes associated protein 1(YAP1)in A549 cells was determined by immunofluorescence.The mRNA and protein levels in NSCLC tissues and cell lines were measured by qRT-PCR and western blot,respectively.Results:Apelin was upregulated in tumor tissues compared with the adjacent tissues.Apelin promoted proliferation,migration,and invasion of A549 and H460 cells,which was reversed by competitive apelin receptor(APJ)antagonist ML221.Additionally,apelin upregulated YAP1 expression,whereas silence of YAP1 by small interfering RNA(siRNA)attenuated apelin-induced cell proliferation,migration and invasion and suppressed epithelial-mesenchymal transition progression.Conclusion:Apelin promotes NSCLC cells proliferation,migration,and invasion by modulating YAP1 and might be a potential therapeutic target for NSCLC treatment.展开更多
文摘Objective To evaluate the correlation between programmed death-ligand 1(PD-L1)expression in primary lung cancer cells,tumor associated macrophages(TAM)and patients’clinicopathological characteristics.Methods From 2008 to 2010,208 non-small cell lung cancer patients who underwent surgery or CT-guided biopsy were recruited from Huadong Hospital,Fudan University.Immunohistochemistry staining was performed to evaluate the PD-L1 expression in both primary lung cancer cells and CD68 positive TAM.The relationship between PD-L1 expression and the clinical pathology was evaluated usingχ2test.Spearman’s rank correlations were used to determine the correlation between PD-L1 expression in tumor cells and macrophages.Results Positive PD-L1 expression in primary cancer cells was found in 136(65.3%)patients,which were negatively correlated with lymph node metastasis(P=0.009)and smoking history(P=0.036).Besides,TAM with PD-L1 expression(found in 116 patients)was positively associated with smoking history(P=0.034),well-differentiation(P=0.029)and negative lymph node metastasis(P=0.0096).A correlation between PD-L1 expression in primary tumor cells and non-small cell lung cancer associated macrophages was found(r=0.228,P=0.021).Conclusion PD-L1,secreted from TAM,might induce cancer cells apoptosis,and decrease lymph node metastasis.
基金the National Natural Science Foundation of China(81872863)the Major Scientific Fund Project of Heilongjiang Province(ZD2019H001).
文摘Background:Apelin,an endogenous ligand of G-protein coupled receptor(GPCR),is a secreted peptide involved in the development of various tumors.However,the relationship between apelin and non-small cell lung cancer(NSCLC)is not quite clear.This study was designed to investigate the effect and mechanism of apelin on cell proliferation,migration and invasion of NSCLC cells.Methods:Twelve NSCLC specimens were collected for hematoxylin-eosin(HE)staining and immunohistochemistry analyses.Cell proliferation was examined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)and cell migration and invasion were assessed using wound-healing and transwell assays.The subcellular location of yes associated protein 1(YAP1)in A549 cells was determined by immunofluorescence.The mRNA and protein levels in NSCLC tissues and cell lines were measured by qRT-PCR and western blot,respectively.Results:Apelin was upregulated in tumor tissues compared with the adjacent tissues.Apelin promoted proliferation,migration,and invasion of A549 and H460 cells,which was reversed by competitive apelin receptor(APJ)antagonist ML221.Additionally,apelin upregulated YAP1 expression,whereas silence of YAP1 by small interfering RNA(siRNA)attenuated apelin-induced cell proliferation,migration and invasion and suppressed epithelial-mesenchymal transition progression.Conclusion:Apelin promotes NSCLC cells proliferation,migration,and invasion by modulating YAP1 and might be a potential therapeutic target for NSCLC treatment.
