RESUMO
OBJECTIVE: To detect the expression of RING finger protein 135 (RNF135) in lung adenocarcinoma tissues and explore its role in the progression of lung adenocarcinoma. METHODS: Bioinformation analysis, quantitative polymerase chain reaction, and immunoblotting technique discovered the expression of RNF135 in lung adenocarcinoma tissues. Cell counting kit-8 and colony formation, immunostaining, and immunoblot assays examined the effects of RNF135 on cell growth and autophagy. Co-immunoprecipitation (Co-IP), immunostaining, and immuoblotting were conducted to confirm the mechanism. RESULTS: RNF135 was highly expressed in lung adenocarcinoma. In addition, RNF135 promoted lung adenocarcinoma cell growth. Further, data confirmed that RNF135 promoted autophagy in lung adenocarcinoma cells. Mechanically, RNF135 directly interacted with Unc-51-like autophagy activating kinase 1 (ULK1) to promote its phosphorylation level. CONCLUSION: RNF135 promoted cell growth and autophagy in lung adenocarcinoma by promoting the phosphorylation of ULK1.
Assuntos
Adenocarcinoma de Pulmão , Neoplasias Pulmonares , Ubiquitina-Proteína Ligases , Humanos , Autofagia , Proteína Homóloga à Proteína-1 Relacionada à Autofagia/metabolismo , Proliferação de Células , Peptídeos e Proteínas de Sinalização Intracelular/genética , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Peptídeos e Proteínas de Sinalização Intracelular/farmacologia , Neoplasias Pulmonares/patologia , Fosforilação , Ubiquitina-Proteína Ligases/genética , Ubiquitina-Proteína Ligases/metabolismo , Ubiquitina-Proteína Ligases/farmacologiaRESUMO
The purpose of this study was to explore the regulatory mechanism of Annexin A1 (ANXA1) in glioma cells in the inflammatory microenvironment induced by tumour necrosis factor α (TNF-α) and its effects on glioma cell proliferation. CCK-8 analysis demonstrated that TNF-α stimulation promotes rapid growth in glioma cells. Changes in tumour necrosis factor receptor 1 (TNFR1) and ANXA1 expression in glioma cells stimulated with TNF-α were revealed through western blot analysis and immunofluorescence staining. Coimmunoprecipitation analysis revealed that ANXA1 interacts with TNFR1. Moreover, we found that ANXA1 promotes glioma cell growth by activating the p65 and Akt signalling pathways. Finally, immunohistochemistry analysis showed an obvious correlation between ANXA1 expression and Ki-67 in glioma tissues. In summary, our results indicate that the TNF-α/TNFR1/ANXA1 axis regulates the proliferation of glioma cells and that ANXA1 plays a regulatory role in the inflammatory microenvironment.
RESUMO
The aim of this research was to investigate the role of hyaluronan-binding protein 1 (HABP1) in lung adenocarcinoma. It was demonstrated by bioinformatics analysis that HABP1 was one of the differentially expressed genes in lung adenocarcinoma. Then, it was confirmed by qPCR, western blot, and immunohistochemistry analysis that HABP1 was upregulated in human tissue specimens we collected. Survival analysis showed that HABP1 was promised to serve as a new biomarker to predict the progress and prognosis of lung adenocarcinoma patients. In addition, we further studied the effects of regulating the expression of HABP1 on lung adenocarcinoma cells, indicating that altered expression of HABP1 could adjust cell proliferation and invasion through the NFκB signaling pathway.