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Role of IKK alpha in skin squamous cell carcinomas

  1. Author:
    Park, E. M.
    Liu, B. G.
    Xia, X. J.
    Zhu, F.
    Jami, W. B.
    Hu, Y. L.

  2. Author Address

    [Jami, Willette-Brown; Hu, Yinling] NCI, Canc & Inflammat Program, Ctr Canc Res, NIH, Frederick, MD 21701 USA. [Park, Eunmi] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA. [Liu, Bigang; Zhu, Feng] Univ Texas MD Anderson Canc Ctr, Dept Carcinogenesis, Smithville, TX 78957 USA. [Xia, Xiaojun] Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.;Hu, YL, NCI, Canc & Inflammat Program, Ctr Canc Res, NIH, Frederick, MD 21701 USA.;huy2@mail.nih.gov
    1. Year: 2011
    2. Date: Jan
  2. Journal: Future Oncology
    1. 7
    2. 1
    3. Pages: 123-134
  4. Type of Article: Review
  5. ISSN: 1479-6694
  1. Abstract:

    Squamous cell carcinoma (SCC) and basal cell carcinoma (BCC) are two major types of skin cancer derived from keratinocytes. SCC is a more aggressive type of cancer than BCC in humans. One significant difference between SCC and BCC is that SCC development is generally associated with cell dedifferentiation and morphological changes. When SCC is converted to spindle cell carcinoma, the latest stage of cancer, the tumor cells change to a fibroblastic cell morphology (epithelial-to-mesenchymal transition) and lose their differentiation markers. Recently, several laboratories have reported altered I kappa B kinase alpha (IKK alpha) protein localization, downregulated IKK alpha, and IKK alpha gene deletions and mutations in human SCCs of the skin, lung, esophagus, and neck and head. In addition, IKK alpha reduction promotes chemical carcinogen- and ultraviolet B-induced skin carcinogenesis, and IKK alpha deletion in keratinocytes causes spontaneous skin SCCs, but not BCCs, in mice. Thus, IKK alpha emerges as a bona fide skin tumor suppressor. In this article, we will discuss the role of IKK alpha in skin SCC development.

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External Sources

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  2. DOI: 10.2217/fon.10.166
  3. View record in Web of Science®
  4. WOS: 000287173900014

Library Notes

  1. Fiscal Year: FY2010-2011
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