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NF-?B inducing kinase, a central signaling component of the non-canonical pathway of NF-?B, contributes to ovarian cancer progression.

ABSTRACT: Ovarian cancer is one of the leading causes of female death and the development of novel therapeutic approaches is urgently required. Nuclear factor-?B (NF-?B) is constitutively activated in several types of cancer including ovarian cancer and is known to support the survival of cancer cells. However, molecular mechanisms of persistent activation of NF-?B in ovarian cancer remain largely unknown. We report here that, in addition to the previously reported canonical activation, NF-?B is activated through the noncanonical pathway in ovarian cancer cells. RNA interference-mediated silencing of NF-?B inducing kinase (NIK), a central regulator of the noncanonical pathway, reduced the NF-?B2/p52 DNA binding activity and NF-?B-dependent reporter gene expression as well as NF-?B target gene expression. Notably, anchorage-dependent and -independent cell growth was impaired in NIK-depleted cells. Depletion of NIK also suppressed tumor formation in the nude mouse xenograft assay. These results indicate that NIK plays a key role in constitutive NF-?B activation and the progression of ovarian cancer cells and suggest that NIK represents an attractive therapeutic target for ovarian cancer.

SUBMITTER: Uno M 

PROVIDER: S-EPMC3922808 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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NF-κB inducing kinase, a central signaling component of the non-canonical pathway of NF-κB, contributes to ovarian cancer progression.

Uno Masaya M   Saitoh Yasunori Y   Mochida Kanako K   Tsuruyama Eri E   Kiyono Tohru T   Imoto Issei I   Inazawa Johji J   Yuasa Yasuhito Y   Kubota Toshiro T   Yamaoka Shoji S  

PloS one 20140212 2

Ovarian cancer is one of the leading causes of female death and the development of novel therapeutic approaches is urgently required. Nuclear factor-κB (NF-κB) is constitutively activated in several types of cancer including ovarian cancer and is known to support the survival of cancer cells. However, molecular mechanisms of persistent activation of NF-κB in ovarian cancer remain largely unknown. We report here that, in addition to the previously reported canonical activation, NF-κB is activated  ...[more]

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