Research Papers:

miR-130b, an onco-miRNA in bladder cancer, is directly regulated by NF-κB and sustains NF-κB activation by decreasing Cylindromatosis expression

Xiaolu Cui, Chuize Kong _, Yuyan Zhu, Yu Zeng, Zhe Zhang, Xiankui Liu, Bo Zhan, Chiyuan Piao and Zhenming Jiang

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Oncotarget. 2016; 7:48547-48561. https://doi.org/10.18632/oncotarget.10423

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Xiaolu Cui1, Chuize Kong1, Yuyan Zhu1, Yu Zeng1, Zhe Zhang1, Xiankui Liu1, Bo Zhan1, Chiyuan Piao1, Zhenming Jiang1

1Department of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China

Correspondence to:

Chuize Kong, email: [email protected]

Keywords: bladder transitional cell carcinoma, NF-κB, miR-130b, CYLD

Received: January 28, 2016    Accepted: May 22, 2016    Published: July 06, 2016


Persistent activation of NF-κB signaling is closely related to chronic inflammation and tumorigenesis. Commonly, NF-κB signaling is tightly controlled by multiple feedback loops and regulators, such as the deubiquitinases (DUBs). However, in cancer cells, NF-κB 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-κB 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-κB signaling, miR-130b can in return sustain the persistent activation of NF-κB, which may promote the malignant progression of TCC. Thus, the present study uncovers a potential signaling transduction in which NF-κB is continuously activated, and may provide a novel therapeutic approach for the clinical management of TCC.

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