scholarly journals Heparin-binding epidermal growth factor-like growth factor isoforms and epidermal growth factor receptor/ErbB1 expression in bladder cancer and their relation to clinical outcome

Cancer ◽  
2007 ◽  
Vol 109 (10) ◽  
pp. 2016-2024 ◽  
Author(s):  
Christopher Kramer ◽  
Kai Klasmeyer ◽  
Hans Bojar ◽  
Wolfgang A. Schulz ◽  
Rolf Ackermann ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Clinical Outcome ◽  
Growth Factor Receptor ◽  
Heparin Binding ◽  
Epidermal Growth

scholarly journals miR-202 Inhibits Cell Proliferation, Migration, and Invasion by Targeting Epidermal Growth Factor Receptor in Human Bladder Cancer

2018 ◽  
Vol 26 (6) ◽  
pp. 949-957 ◽  
Author(s):  
Liqing Zhang ◽  
Jianjiang Xu ◽  
Gaodi Yang ◽  
Heng Li ◽  
Xiuxia Guo
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Epidermal Growth

Recent studies have demonstrated that miR-202 is associated with several types of cancer; however, the expression and function of miR-202 have not been investigated in bladder cancer. We analyzed the expression of miR-202 in bladder cancer tissues and adjacent noncancerous tissues. The effect of miR-202 on the proliferation, migration, and invasion was evaluated by in vitro assays. The target gene of miR-202 was assessed by luciferase reporter assay. In this study, miR-202 was found to be significantly downregulated in bladder cancer cell lines and tissues and was highly correlated with the T classification, N classification, grade, and recurrence. Ectopic expression of miR-202 suppressed cell viability, colony formation, cell migration, and invasion in vitro and inhibited xenograft tumor growth in vivo. Inversely, downregulation of miR-202 had contradictory effects. The 3′-untranslated region (3′-UTR) of epidermal growth factor receptor (EGFR) was identified as a direct target of miR-202 using luciferase reporter assays, and knockdown of EGFR enhanced miR-202-inhibited cell proliferation, migration, and invasion. In conclusion, miR-202 suppresses bladder cancer carcinogenesis and progression by targeting EGFR, thereby representing a potential target for miRNA-based therapy for bladder cancer in the future.

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