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UBC9 coordinates inflammation affecting development of bladder cancer
Xiaoliang Huang1,2,3, Yuting Tao1,2,3, Jiamin Gao1,2,3
1Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.
Scientific Reports
|November 27, 2020
Summary
UBC9, crucial for sumoylation, shows a dual role in bladder cancer. Its absence activates inflammation and promotes cancer stem cells, despite initial up-regulation in tumors.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Sumoylation dysregulation is linked to cancer development.
- UBC9 is the primary enzyme in sumoylation, essential for cellular homeostasis.
- The role of UBC9 in bladder cancer pathogenesis is not well understood.
Purpose of the Study:
- To investigate the clinical significance and functional role of UBC9 in bladder cancer.
- To elucidate the molecular mechanisms underlying UBC9's function in bladder cancer.
Main Methods:
- Immunohistochemistry to assess UBC9 expression.
- UBC9 knockdown and SUMO inhibition followed by cell proliferation, migration, and cell cycle assays.
- RNA sequencing, bioinformatic analysis, cytokine array, and mass cytometry (CyTOF) to explore mechanisms and cell populations.
Main Results:
- UBC9 was upregulated in bladder cancer but inversely correlated with TNM stage and grade.
- UBC9 knockdown led to inflammatory gene activation, inhibited proliferation, and induced apoptosis.
- IL6 was identified as a hub gene, and its upregulation upon UBC9 knockdown activated CD44, a cancer stem cell marker.
Conclusions:
- UBC9 plays a dual role in bladder cancer, maintaining high sumoylation to suppress inflammation.
- Loss of UBC9 promotes inflammation, epithelial-mesenchymal transition, and cancer stem cell formation, contributing to cancer progression.
- UBC9 is critical for modulating inflammatory signaling and maintaining cellular stress responses in bladder cancer.
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