Effect Of LL-37 On Autophagy In Lung Cancer Cells

In recent decades,year by year.It has great significance to study and explore its pathogenesis and process.Autophagy is a highly conserved catabolic process that degrades a bulk of misfolded or damaged proteins and organelles.It plays a very important role in the body's stability,internal environment stability,environmental adaptation.Autophagy plays an important role in maintaining the metabolism and developing tumor cells.In addition,autophagy is also directly involved in the inflammatory immune response process.Antibacterial peptides play a major role in the immune response,with direct antibacterial and a variety of regulatory functions.Antibacterial peptides have direct antibacterial and multiple regulatory functions during the immune response.Cathelicidin is a major family of antimicrobial peptides.The human cathelicidin gene,CAMP,is isolated from human cells and codes for human cationic antimicrobial peptide-18(hCAP-18)/LL-37.The Cnlp gene codes for the cathelicidin-related AMP(CRAMP)peptide in mice,which is similar to the LL-37 peptide in humans.In addition to combating microorganisms,cathelicidin plays a role in various immune functions,including immune modulation,inflammatory reactions,cell proliferation,angiogenesis and inhibition of apoptosis.In HE staining and tumor number statistics experiment,it was observed that the number of lung tumors in mice which knocked out CRAMP was less than the number of lung tumors in C57 mice.This shows that CRAMP promotes the proliferation of lung tumors.At the same time,H1975 human lung cancer cells were cultured 0,0.05,0.5,1,5,and 10 ?g/mL,and CCK8 was used to detect cell proliferation.LL-37 was found to promote proliferation of lung cancer cells,1 ?g/ml were the optimal concentration.Due to the close relationship between inflammation and autophagy,it is speculated that the proliferation may be related to autophagy.So detection of autophagy markers in tumor tissues of two groups of mice,it revealed differences in expression.Compared with the two groups of mice,it shows that the expression of LC3 B and Beclin-1 in lung tumors of C57 mice was higher than that in C57 mice,the expression of P62 is opposite to them.This result indicates that the autophagy in lung tumors of C57 mice is higher,CRAMP can promote autophagy in mouse lung tumors.At the same time,H1975 human lung cancer cells were stimulated with LL-37,1 ?g/ml,0h,24 h,and 48 h were selected.The results of western blotting and cellular immunofluorescence experiments showed that autophagy occurred at 24 h and 48 h,but the effect of 24 h is higher than 48 h.This shows that LL-37 can promote autophagy in lung cancer cells.To ensure the integrity of LL-37 on autophagy in lung cancer cells,the inhibitors chloroquine(CQ)and 3-methyladenine(3-MA)were used.The ratio of LC3-II/?-Actin of the inhibitor chloroquine(CQ)experimental group was higher than the control group,and the experimental group containing 3-methyladenine(3-MA),the ratio of LC3-II/?-Actin is lowered.This result indicates that LL-37 is fully activated in the autophagy process of lung cancer cell H1975.The effect of LL-37 on autophagy has provided new ideas for the study of tumor therapy.While exploring the mechanism between inflammation and tumors,it could consider the relation between inflammation and autophagy,or autophagy and tumors,which may become new breakthroughs in the treatment of cancer.