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Authors Chen W, Zhao K, Miao C, Xu A, Zhang J, Zhu J, Su S, Wang Z
Received 13 December 2016
Accepted for publication 11 February 2017
Published 9 March 2017 Volume 2017:10 Pages 1503—1512
DOI https://doi.org/10.2147/OTT.S130139
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Akshita Wason
Peer reviewer comments 2
Editor who approved publication: Dr Samir Farghaly
Abstract: The evolutionarily conserved genes that encode the tripartite motif
(TRIM) protein family are involved in various biological processes, including
cellular immunity, inflammatory reaction, antiviral activity, and tumor
progression. One member of this protein family, Trim59, has been reported as a
novel biomarker for the occurrence and progression of multiple human
carcinomas, such as lung cancer, gastric cancer, cervical cancer, and
osteosarcoma. However, little is known about the relationship between Trim59
and bladder carcinogenesis. In this study, we examined the expression of Trim59
in bladder cancer (Bca) specimens and cell lines, and investigated its
biological roles in Bca cell lines. We found that Trim59 was upregulated in Bca
tissues and cell lines. In addition, using transwell chamber assays and the
cell scratch test, we determined that knockdown of Trim59 significantly
inhibited the epithelial-mesenchymal transition (EMT) and the processes of cell
invasion and migration in Bca cell lines. Furthermore, we found that
downregulated Trim59 expression could also inhibit cell proliferation and
promote apoptosis. As a result, we demonstrated that the effects of
Trim59-induced EMT and invasion/migration in Bca cells were achieved by the
activation of the transforming growth factor beta/Smad2/3 signaling pathway.
Our findings also revealed that Trim59 can present oncogenic activity, and may
serve as a novel candidate target for bladder carcinoma treatment.
Keywords: Trim59, bladder carcinoma, EMT,
metastasis, TGF-β, Smad2/3