Ubiquitination Degraded BMPR2 By Smurf1 Promotes Bladder Cancer Cell Growth

Author:

Su Qiongli1ORCID,Huang Li2,Guo Ying2,Wei Long2,Wu Ling2,Tan Qiuhong2

Affiliation:

1. Zhuzhou Hospital Affiliated to Central South University: Zhuzhou Central Hospital

2. Zhuzhou Central Hospital

Abstract

Abstract Bladder cancer (BC) is one of the most frequent malignancy cancers in the urinary system worldwide. It has high mortality because chemotherapy and surgery are only effective to very limited BC patients. Thus, developing novel treatment options has become an urgent need to improve clinical outcomes and the quality of life for BC patients. In this study, we proved that BMPR2 degraded by ubiquitin ligase Smad ubiquitination regulator 1 (Smurf1) can promote BC cell growth. Firstly, we detected the interaction relationship between Smurf1 and BMPR2 by CO-IP and bioinformatics tools. Next, transfection lentiviral vectors Plasmids or siRNA was used to over-express or knock-down for Smurf1 in BC cells. Finally, CCK-8 and colony assay were used to detect the growth and proliferation of BC cells J82 and UMUC3. The results demonstrated that Smurf1 plays an essential role in the Smurf1/BMPR2 signaling pathway in J82 and UMUC3 cell growth. Moreover, BMPR2 has a negative correlation with Smurf1 in BC. Additionally, Smurf1 specifically targets BMPR2 and promotes the BMPR2 degradation through the ubiquitin-protease pathway. In summary, Smurf1 may play an important role in the treatment of BC and may be a potential novel target for BC.

Publisher

Research Square Platform LLC

Reference30 articles.

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