NLRC5 Promotes Proliferation Of Endometrial Cancer Cells By Inhibiting Autophagy

Endometrial cancer(EC),one of the most common cancers of the female reproductive system,is the sixth leading cause of cancer death and is on the rise in young women.Recent studies have found that NLR family containing CARD structure domain5(NOD like receptor(NLR)family,caspase recruitment(CARD)domaincontaining5,NLRC5)plays an important role in the development and progression of tumors,and the level of NLRC5 is related to the incidence and survival rate of cancer patients.However,the role of NLRC5 in endometrial cancer and its mechanism are still unclear.Domestic and foreign scholars have found that autophagy can participate in the regulation of NLRs.Numerous studies have confirmed the close relationship between autophagy and tumors and autophagy has a potential role in the treatment of tumors.However,whether autophagy participates in the regulation of NLRC5 has not been reported in the literature.Therefore,this study is to explore whether NLRC5 plays a role in endometrial cancer cells by regulating autophagy,in order to provide a new target for the treatment of this disease.Objective To investigate the expression of NOD like receptor(NLR)family,caspase recruitment(CARD)domaincontaining 5,NLRC5 in endometrial cancer tissues.To preliminarily explore the effect of NLRC5 on the proliferation of AN3 CA in endometrial cancer cells and its mechanism,so as to provide a new basis for the treatment of this disease.Methods1.We selected 20 specimens of endometrial adenocarcinoma surgically removed from patients with endometrial cancer and 20 cases of normal endometrial specimens in outpatient pathology.The protein expression of NLRC5 and autophagy-related proteins Beclin1,LC3 in Endometrial cancer tissue and normal endometrial tissue specimens were observed by immunohistochemistry.Expression of NLRC5 and autophagy-related proteins Beclin1,LC3 in endometrial carcinoma and normal endometrial tissue specimens were detected by Western blot and q RT-PCR.2.NLRC5 plasmid transfection was mediated by clusterplus reagent,and the efficiency of NLRC5 transfection was verified by q RT-PCR and Western blot and inverted fluorescence microscopy.Western blot and q RT-PCR were used to detect the expression of NLRC5 and autophagy-related proteins Beclin1 and LC3 in endometrial carcinoma AN3 CA cells.3.Proliferation of AN3 CA cells was detected by the method of cck-8.Results1.Immunohistochemistry and Western blot showed that the expression of NLRC5 protein was down-regulated and the expression of autophagy-related proteins Beclin1 and LC3 was up-regulated in endometrial carcinoma tissues compared with normal endometrial tissues(p<0.05).2.After transfection of NLRC5 plasmid,Western blot analysis showed that the protein expression levels of autophagy proteins Beclin1 and LC3 were significantly down-regulated in the transfected group compared with the untransfected group(p<0.05).3.After transfection of NLRC5 plasmid,the results of CCK-8 showed that the transfection group significantly increased cell proliferation compared with the untransfected group(p<0.05).4.After transfecting NLRC5 plasmid and adding autophagy agonist rapamycin,cck-8results showed that cell proliferation was significantly increased in transfected NLRC5 plasmid group compared with untransfected NLRC5 plasmid group(p<0.05);Compared with the NLRC5 plasmid group,the autophagy level was increased,but the cell proliferation was significantly decreased(p<0.05).Conclusion The expression of NLRC5 in endometrial cancer cells is significantly lower than that in normal endometrial cells.Overexpression of NLRC5 gene can significantly reduce the level of autophagy in cells and promote the proliferation of endometrial cancer cells.Therefore,NLRC5 may promote the proliferation of endometrial cancer cells by inhibiting autophagy.