scholarly journals miRNA‑373 promotes urinary bladder cancer cell proliferation, migration and invasion through upregulating epidermal growth factor receptor

2018 ◽  
Author(s):  
Yibing Wang ◽  
Zhenqun Xu ◽  
Xia Wang
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Urinary Bladder ◽  
Growth Factor Receptor ◽  
Urinary Bladder Cancer ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
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.

scholarly journals DNA Topoisomerase I Is a Cofactor for c-Jun in the Regulation of Epidermal Growth Factor Receptor Expression and Cancer Cell Proliferation

2005 ◽  
Vol 25 (12) ◽  
pp. 5040-5051 ◽  
Author(s):  
Antoine Mialon ◽  
Matti Sankinen ◽  
Henrik Söderström ◽  
Teemu T. Junttila ◽  
Tim Holmström ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Topoisomerase I ◽  
Growth Factor Receptor ◽  
Dna Topoisomerase I ◽  
Cancer Cell Proliferation ◽  
Dna Topoisomerase ◽  
Epidermal Growth

ABSTRACT DNA topoisomerase I (Topo I) is a molecular target for the anticancer agent topotecan in the treatment of small cell lung cancer and ovarian carcinomas. However, the molecular mechanisms by which topotecan treatment inhibits cancer cell proliferation are unclear. We describe here the identification of Topo I as a novel endogenous interaction partner for transcription factor c-Jun. Reciprocal coimmunoprecipitation analysis showed that Topo I and c-Jun interact in transformed human cells in a manner that is dependent on JNK activity. c-Jun target gene epidermal growth factor receptor (EGFR) was identified as a novel gene whose expression was specifically inhibited by topotecan. Moreover, Topo I overexpression supported c-Jun-mediated reporter gene activation and both genetic and chemical inhibition of c-Jun converted cells resistant to topotecan-elicited EGFR downregulation. Topotecan-elicited suppression of proliferation was rescued by exogenously expressed EGFR. Furthermore, we demonstrate the cooperation of the JNK-c-Jun pathway, Topo I, and EGFR in the positive regulation of HT-1080 cell proliferation. Together, these results have identified transcriptional coactivator Topo I as a first endogenous cofactor for c-Jun in the regulation of cell proliferation. In addition, the results of the present study strongly suggest that inhibition of EGFR expression is a novel mechanism by which topotecan inhibits cell proliferation in cancer therapy.

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