NF-κB induces abnormal centrosome amplification by upregulation of CDK2 in laryngeal squamous cell cancer

Liu, Jianli; Ma, Hui‐Ping; Lu, Xiu-Li; Guo, Xing Rong; Li, Fucai

doi:10.3892/ijo.2011.1125

Cited by 18 publications

(23 citation statements)

References 32 publications

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“…This might be an important link between K8 downregulation and increased sensitivity of A431 cells toward apoptotic stimuli. Aside from this, upregulation in 14-3-3c levels and decreased NF-jB activity, further supports this hypothesis [68,69].…”

Section: Discussionsupporting

confidence: 73%

Depletion of keratin 8/18 modulates oncogenic potential by governing multiple signaling pathways

et al. 2018

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Section: Discussionsupporting

confidence: 73%

Depletion of keratin 8/18 modulates oncogenic potential by governing multiple signaling pathways

et al. 2018

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“…These observations and the experimental studies linking hypoxia, IRR, and tumor progression have suggested new strategies for preventing tumors, reducing their incidence, slowing their progression, substantially increasing survival, and decreasing death ratio for malignancy (Liu et al, 2011). …”

Section: Hypoxia and Inflammation In Cancer Progression Generation Omentioning

confidence: 99%

Modulators of HIF1α and NFkB in Cancer Treatment: Is it a Rational Approach for Controlling Malignant Progression?

Tafani¹,

Pucci²,

Russo³

et al. 2013

Front. Pharmacol.

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HIF1α and NFkB are two transcription factors very frequently activated in tumors and involved in tumor growth, progression, and resistance to chemotherapy. In fact, HIF1α and NFkB together regulate transcription of over a thousand genes that, in turn, control vital cellular processes such as adaptation to the hypoxia, metabolic reprograming, inflammatory reparative response, extracellular matrix digestion, migration and invasion, adhesion, etc. Because of this wide involvement they could control in an integrated manner the origin of the malignant phenotype. Interestingly, hypoxia and inflammation have been sequentially bridged in tumors by the discovery that alarmin receptors genes such as RAGE, P2X7, and some TLRs, are activated by HIF1α; and that, in turn, alarmin receptors strongly activate NFkB and proinflammatory gene expression, evidencing all the hallmarks of the malignant phenotype. Recently, a large number of drugs have been identified that inhibit one or both transcription factors with promising results in terms of controlling tumor progression. In addition, many of these molecules are natural compounds or off-label drugs already used to cure other pathologies. Some of them are undergoing clinical trials and soon they will be used alone or in combination with standard anti-tumoral agents to achieve a better treatment of tumors with reduction of metastasis formation and, more importantly, with a net increase in survival. This review highlights the central role of HIF1α activated in hypoxic regions of the tumor, of NFkB activation and proinflammatory gene expression in transformed cells to understand their progression toward malignancy. Different molecules and strategies to inhibit these transcription factors will be reviewed. Finally, the central role of a new class of deacetylases called Sirtuins in regulating HIF1α and NFkB activity will be outlined.

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“…The transcription factor NF-jB is a major regulator of CDK2 expression (Liu et al, 2011) and ICAM-1 expression (Melotti et al, 2001). Therefore, we evaluated the levels of CDK2 and ICAM-1 in splenocytes.…”

Section: Asd Activates Nf-jb In Cd4 1 and Cd11b 1 Cellsmentioning

confidence: 99%

Asian sand dust causes subacute peripheral immune modification with NF-κB activation

et al. 2013

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Asian sand dust (ASD), a type of particulate matter found in Asia, migrates to East Asia. The increased airborne spread of ASD has led to concerns regarding possible adverse health effects. Our group previously reported that ASD induces lung inflammation in mice, but it is still unclear whether ASD affects lymphoid organs. In this study, we investigated the effect of ASD on splenocytes in a mouse model of ASD exposure. ICR mice were intratracheally administered a single dose of normal saline (control) or ASD and were subsequently sacrificed 1 or 3 days later. TNF-α production in bronchoalveolar lavage fluids was higher at day 1, but not at day 3, after ASD administration. The enzyme-linked immunosorbent assay results showed that ASD administration increased mitogen-induced IL-2, TNF-α, and IL-6 production in splenocytes. Additionally, cell viability assay showed enhanced splenocyte proliferation at day 3, but not at day 1, after ASD administration. The electrophoretic mobility shift assay results demonstrated that nuclear factor κB (NF-κB) was activated in splenocytes on day 3, but not on day 1. In particular, NF-κB activation was detected in CD4(+) and CD11b(+) cells on day 3. These results suggest that ASD induces subacute inflammatory responses with NF-κB activation in the spleen, in contrast to acute inflammation in the lungs.

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NF-κB induces abnormal centrosome amplification by upregulation of CDK2 in laryngeal squamous cell cancer

Cited by 18 publications

References 32 publications

Depletion of keratin 8/18 modulates oncogenic potential by governing multiple signaling pathways

Depletion of keratin 8/18 modulates oncogenic potential by governing multiple signaling pathways

Modulators of HIF1α and NFkB in Cancer Treatment: Is it a Rational Approach for Controlling Malignant Progression?

Asian sand dust causes subacute peripheral immune modification with NF-κB activation

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