Journal
ONCOTARGET
Volume 7, Issue 30, Pages 48547-48561Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.10423
Keywords
bladder transitional cell carcinoma; NF-kappa B; miR-130b; CYLD
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Funding
- National Natural Science Foundation of China [81372723]
- Shenyang City Project of Key Laboratory [F13-293-1-00]
- Liaoning Province Science and Technology Project [2012225016]
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Persistent activation of NF-kappa B signaling is closely related to chronic inflammation and tumorgenesis. Commonly, NF-kappa B signaling is tightly controlled by multiple feedback loops and regulators, such as the deubiquitinases (DUBs). However, in cancer cells, NF-kappa B may override these feedbacks through special pathways and lead to the sustained activation. In the present study, we demonstrate that in transitional cell carcinoma (TCC) of bladder, miR-130b plays an oncogenesis role, it enhanced proliferation, invasion and migration of TCC cell, and was highly correlated with tumor progression. On the other hand, NF-kappa B directly regulated the transcription of miR-130b by binding with its promoter region. Importantly, we verify that, through deceasing the expression of Cylindromatosis (CYLD), a K63-specific DUB and endogenous blocker of NF-kappa B signaling, miR-130b can in return sustain the persistent activation of NF-kappa B, which may promote the malignant progression of TCC. Thus, the present study uncovers a potential signaling transduction in which NF-kappa B is continuously activated, and may provide a novel therapeutic approach for the clinical management of TCC.
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