Study Of The Biological Behavior Of Galectin-1 On Lung Adenocarcinoma

Background and purpose of the study:Lung adenocarcinoma has always been one of the top three cancers in terms of incidence and mortality,and it is one of the most common malignant tumors,and because of its high lethality,countries around the world waste a lot of human and material resources every year to treat lung cancer.Therefore,it is important to investigate the molecular mechanism of lung adenocarcinoma development for the diagnosis and treatment of lung adenocarcinoma.Galectin-1 is a member of the galactose lectin family,which is expressed in the nucleus,cytoplasm,inner and outer cell membrane and extracellular matrix,and is involved in apoptosis,proliferation,migration,invasion,adhesion,activation,signaling and inflammation.Since there are few studies in lung adenocarcinoma,we propose to investigate how galectin-1 is involved in regulating the molecular mechanism of lung adenocarcinoma through a series of experiments by knocking down the expression of galectin-1.Methods:Firstly,we collected lung tissues from clinical patients(including cancerous tissues and paraneoplastic normal tissues)to detect the expression of galectin-1 in lung tissues by immunohistochemistry,and used fluorescence quantitative PCR to detect the m RNA expression of galectin-1 in lung cancer tissues and paraneoplastic normal tissues of patients.Lung adenocarcinoma cell lines A549 and H1299 were used as representatives of lung adenocarcinoma and BEAS-2b human normal bronchial epithelial cell line was used as a substitute for normal lung tissue to study the effect of galectin-1 on lung adenocarcinoma at the cellular level,and the m RNA content of galectin-1 in three different cell lines was detected by fluorescence quantitative PCR.The expression of galectin-1 was then knocked down by si-RNA,and the biological behavior of the cells would be confirmed by knocking down galectin-1 using CCK8,scratch,migration,invasion,and flow cytometry experiments.The expression of BAX,BCL-2 and cleaved Caspase3 was examined by Western blot assay after knockdown of galectin-1 compared with the control group,and the relative expression of AKT,p-AKT,ERK,p-ERK and other pathway proteins were observed after knockdown of galectin-1 compared with the control group.compared with the control group.The tumors were removed and the expression of galectin-1 and p-ERK was observed by immunohistochemistry,and then the apoptosis of the tumors was observed by tunel staining.Results:1.Galectin-1 could be found to be more expressed in lung cancer tissues than in normal tissues adjacent to cancer by immunohistochemistry.The m RNA level of galectin-1 was also found to be higher in lung cancer tissues than in normal tissues adjacent to cancer using fluorescent quantitative PCR.2.The m RNA level of galectin-1 in lung adenocarcinoma cells A549 and H1299 could be found to be higher than that in normal bronchial epithelial cells BEAS-2b by fluorescent quantitative PCR.3.galectin-1 inhibited the expression of A549,H1299 by si RNA interference with the expression of galectin-1 inhibited the proliferation,migration,and invasion of A549,H1299 cells promoting their apoptosis.4.Western blot experiments demonstrated that interference with the expression of galectin-1 increased the expression of the apoptosis-promoting related proteins BAX and cleaved Caspase3 compared with the control group,in contrast to In contrast,the expression of BCL-2,a protein that inhibits apoptosis,was decreased,and p-ERK,a related pathway protein,was also activated.5.Subcutaneous tumorigenesis experiments in nude mice with a lentiviral vector low in galectin-1 expression showed that galectin-1 knockdown affected the growth of nude mouse tumors,and p-ERK expression was also decreased in nude mouse tumors,and tunel experiments showed that galectin-1 knockdown promoted the growth of nude mouse tumors.galectin-1 knockdown promoted the apoptosis of tumors.Conclusions:Galectin-1 is a class of genes that promotes cancer development and mediates the biological behavior of lung adenocarcinoma cells through the p-ERK pathway,and that Galectin-1 can be further investigated as an oncogenic gene.