IKK/NF- B signaling: balancing life and death - a new approach to cancer therapy

Luo, Jun-Li; Kamata, Hideaki; Karin, Michael

doi:10.1172/jci26322

Cited by 795 publications

(722 citation statements)

References 118 publications

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“…6 Liberated NF-κB dimers then enter the nucleus where they induce the transcription of various genes. 7,8 There are two NF-κB activation pathways: the classical pathway 6,9 and the alternative pathway. [10][11][12] IKKα contributes to the control of both pathways and functions in the cytoplasm.…”

mentioning

confidence: 99%

IKKα-mediated biogenesis of miR-196a through interaction with Drosha regulates the sensitivity of cancer cells to radiotherapy

et al. 2016

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Radioresistance is a major obstacle in successful clinical cancer radiotherapy, and the underlying mechanisms are not clear. Here we show that IKKα-mediated miR-196a biogenesis via interaction with Drosha regulates the sensitivity of nasopharyngeal carcinoma (NPC) cells to radiotherapy. Phosphorylation of IKKα at T23 site (p-IKKαT23) promotes the binding of IKKα to Drosha that accelerates the processing of miR-196a primary transcripts, leading to increased expressions of both precursor and mature miR-196a. Dephosphorylation of p-IKKαT23 downregulates miR-196a expression and promotes the resistance of NPC cells to radiation treatment. The miR-196a mimic suppresses while its inhibitor promotes the resistance of NPC to radiation treatment. Importantly, the expression of p-IKKαT23 is positively related to the expression of miR-196a in human NPC tissues, and expression of p-IKKαT23 and miR-196a is inversely correlated with NPC clinical radioresistance. Thus, our studies establish a novel mechanistic link between the inactivation of IKKαT23-Drosha-miR-196a pathway and NPC radioresistance, and de-inactivation of IKKαT23-Drosha-miR-196a pathway would be an efficient way to restore the sensitivity of radioresistant NPC to radiotherapy.

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confidence: 99%

IKKα-mediated biogenesis of miR-196a through interaction with Drosha regulates the sensitivity of cancer cells to radiotherapy

et al. 2016

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“…NF-kB inhibition can enhance the susceptibility of a variety of epithelial and hematopoietic malignancies to chemotherapy-induced cell death (Karin et al, 2004;Luo et al, 2005; NF-jB-dependent sensitization to starvation C Fabre et al Braun et al, 2006b). Therefore, we investigated the possibility of sensitizing P39 cells to chemotherapeutic agents by inhibiting IKK with BAY11-7082.…”

Section: Resultsmentioning

confidence: 99%

NF-κB inhibition sensitizes to starvation-induced cell death in high-risk myelodysplastic syndrome and acute myeloid leukemia

et al. 2007

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“…The fi rst group mainly includes inhibitor of apoptosis proteins (IAPs), Ciap1, Ciap2, XIAP and CFLIP (Srinivasula and Ashwell, 2008). The second group mainly refers to Bcl-2 family members, including Bcl-2 and Bcl-xL (Luo et al, 2005).…”

Section: Function Of Stat3 In Inflammation and Cancermentioning

confidence: 99%

NF-κB and STAT3 signaling pathways collaboratively link inflammation to cancer

2013

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IKK/NF- B signaling: balancing life and death - a new approach to cancer therapy

Cited by 795 publications

References 118 publications

IKKα-mediated biogenesis of miR-196a through interaction with Drosha regulates the sensitivity of cancer cells to radiotherapy

IKKα-mediated biogenesis of miR-196a through interaction with Drosha regulates the sensitivity of cancer cells to radiotherapy

NF-κB inhibition sensitizes to starvation-induced cell death in high-risk myelodysplastic syndrome and acute myeloid leukemia

NF-κB and STAT3 signaling pathways collaboratively link inflammation to cancer

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