المؤلفون: Ming Li, Liang Ma, Qunshan Lu, Yuankai Zhang, Jianmin Li, Deqiang Li, Peilai Liu

المصدر: OncoTargets and Therapy. 12:11587-11595

مصطلحات موضوعية: 0301 basic medicine, medicine.diagnostic_test, Immunoprecipitation, Autophagy, Biology, medicine.disease, Embryonic stem cell, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Real-time polymerase chain reaction, Oncology, Ubiquitin, Western blot, 030220 oncology & carcinogenesis, medicine, Cancer research, biology.protein, Neoplasm, Pharmacology (medical), Sarcoma

الوصف: Background and aim Ewing sarcoma (ES) is an aggressive neoplasm predominantly occurring in adolescents and has a poor prognosis when metastasized. In the current study, we were aiming to investigate the function of TRIM3 in autophagy in ES cells. Methods The expression of TRIM3 in Ewing sarcoma tissues and normal tissues was examined by quantitative PCR and western blot. The effect of TRIM3 on autophagy was detected by western blot and immunofluorescence assay. Target of TRIM3 was examined by western blot, immunoprecipitation and ubiquitination assay. Results We found the expression of TRIM3 was significantly up-regulated in Ewing sarcoma tissues compared with normal tissues, and this phenomenon was regulated by EWS-FLI1 expression. Furthermore, we observed that overexpression of TRIM3 markedly and consistently inhibited autophagy in ES cells, and autophagy was enhanced in TRIM3-silenced ES cells. Finally, we found in ES cells, TRIM3 could directly interact with Beclin1, and improved its K48-linked polyubiquitinaion, leading to the degradation of Beclin1 and then regulated autophagy. Conclusion In the present research, for the first time we revealed that TRIM3 negatively regulates autophagy through promoting degradation of Beclin1 in Ewing sarcoma cells, and these findings may provide ideas for ES research.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::a3c6fd0f852b99c0ebece69580b58670
https://doi.org/10.2147/ott.s219777

المؤلفون: Qunshan, Lu, Yuankai, Zhang, Liang, Ma, Deqiang, Li, Ming, Li, Peilai, Liu, Jianmin, Li

المصدر: OncoTargets and therapy

مصطلحات موضوعية: autophagy, Beclin1, TRIM3, Ewing sarcoma, Original Research

الوصف: Background and aim Ewing sarcoma (ES) is an aggressive neoplasm predominantly occurring in adolescents and has a poor prognosis when metastasized. In the current study, we were aiming to investigate the function of TRIM3 in autophagy in ES cells. Methods The expression of TRIM3 in Ewing sarcoma tissues and normal tissues was examined by quantitative PCR and western blot. The effect of TRIM3 on autophagy was detected by western blot and immunofluorescence assay. Target of TRIM3 was examined by western blot, immunoprecipitation and ubiquitination assay. Results We found the expression of TRIM3 was significantly up-regulated in Ewing sarcoma tissues compared with normal tissues, and this phenomenon was regulated by EWS-FLI1 expression. Furthermore, we observed that overexpression of TRIM3 markedly and consistently inhibited autophagy in ES cells, and autophagy was enhanced in TRIM3-silenced ES cells. Finally, we found in ES cells, TRIM3 could directly interact with Beclin1, and improved its K48-linked polyubiquitinaion, leading to the degradation of Beclin1 and then regulated autophagy. Conclusion In the present research, for the first time we revealed that TRIM3 negatively regulates autophagy through promoting degradation of Beclin1 in Ewing sarcoma cells, and these findings may provide ideas for ES research.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=pmid________::2ac60a59227b2b62157a7019d7539ff1
https://pubmed.ncbi.nlm.nih.gov/32021240