Journal
TUMOR BIOLOGY
Volume 37, Issue 9, Pages 12731-12742Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1007/s13277-016-5157-0
Keywords
Gemcitabine; Cylindromatosis (CYLD); Livin; Bladder cancer (BCa); Autophagy
Categories
Funding
- Shandong Key Research and Development Project [2015GSF118055]
- Medicine and Healthcare Technology Development Project of Shandong Province [2014WS0341]
- Natural Science Foundation of Shandong Province [2014ZRB14513, 2014ZRB14081]
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Although GC (gemcitabine and cisplatin) chemotherapy remains an effective method for treating bladder cancer (BCa), chemoresistance is a major obstacle in chemotherapy. In this study, we determined whether gemcitabine resistance correlates with migratory/invasive potential in BCa and whether this relationship is regulated by the cylindromatosis (CYLD)-Livin module. First, we independently investigated the correlation of CYLD/Livin and gemcitabine resistance with the potential for tumor migration and invasiveness. Second, we found that co-transfected CYLD and Livin dramatically improved sensitivity to gemcitabine chemotherapy and decreased migration/invasion potential. Next, we determined that CYLD may regulate Livin by the NF-kappa B-dependent pathway. We also found that CYLD overexpression and Livin knockdown might improve gemcitabine chemosensitivity by decreasing autophagy and increasing apoptosis in BCa cells. Finally, the effects of CYLD-Livin on tumor growth in vivo were evaluated. Our study demonstrates that CYLD-Livin might represent a potential therapeutic for chemoresistant BCa.
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