Inhibitor-κB Kinase in Tumor Promotion and Suppression During Progression of Squamous Cell Carcinoma
Open Access
- 1 September 2007
- journal article
- editorial
- Published by American Association for Cancer Research (AACR) in Clinical Cancer Research
- Vol. 13 (17) , 4956-4959
- https://doi.org/10.1158/1078-0432.ccr-07-1287
Abstract
Previous studies have provided evidence that activation of inhibitor-κB kinases (IKK) leads to nuclear translocation and activation of nuclear factor-κB (NF-κB), a transcription factor that can promote cell survival and malignant phenotypic changes important in development and progression ofThis publication has 27 references indexed in Scilit:
- Normal epidermal differentiation but impaired skin-barrier formation upon keratinocyte-restricted IKK1 ablationNature Cell Biology, 2007
- A critical role for IκB kinase α in the development of human and mouse squamous cell carcinomasProceedings of the National Academy of Sciences, 2006
- Gene Expression Profiles Identify Epithelial-to-Mesenchymal Transition and Activation of Nuclear Factor-κB Signaling as Characteristics of a High-risk Head and Neck Squamous Cell CarcinomaCancer Research, 2006
- Protein Kinase Casein Kinase 2 Mediates Inhibitor-κB Kinase and Aberrant Nuclear Factor-κB Activation by Serum Factor(s) in Head and Neck Squamous Carcinoma CellsCancer Research, 2006
- Alternative pathways of NF-κB activation: A double-edged sword in health and diseaseCytokine & Growth Factor Reviews, 2006
- Nuclear factor-κB in cancer development and progressionNature, 2006
- Role of TGFβ in skin inflammation and carcinogenesisMolecular Carcinogenesis, 2006
- IκB Kinase α and p65/RelA Contribute to Optimal Epidermal Growth Factor-induced c-fos Gene Expression Independent of IκBα DegradationPublished by Elsevier ,2004
- IκB kinase-α acts in the epidermis to control skeletal and craniofacial morphogenesisNature, 2004
- Expression of proangiogenic chemokine Gro 1 in low and high metastatic variants of Pam murine squamous cell carcinoma is differentially regulated by IL-1?, EGF and TGF-?1 through NF-?B dependent and independent mechanismsInternational Journal of Cancer, 2001