Journal Article

Suppressive function of RKTG on chemical carcinogen-induced skin carcinogenesis in mouse

Xiaoduo Xie, Yixuan Zhang, Yuhui Jiang, Weizhong Liu, Hong Ma, Zhenzhen Wang and Yan Chen

in Carcinogenesis

Volume 29, issue 8, pages 1632-1638
Published in print August 2008 | ISSN: 0143-3334
Published online June 2008 | e-ISSN: 1460-2180 | DOI:
Suppressive function of RKTG on chemical carcinogen-induced skin carcinogenesis in mouse

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Raf kinase trapping to Golgi (RKTG) is a newly characterized negative regulator of the Ras–Raf—MEK–ERK signaling pathway via sequestrating Raf-1 to the Golgi apparatus. However, little is known about the physiological functions of RKTG in mitogenic pathway and carcinogenesis. Here, we describe a suppressive role of RKTG in skin carcinogenesis by analyzing chemical carcinogen-induced tumorigenesis. Epidermis hyperplasia and proliferation are increased in RKTG-deficient mice (RKTG−/−) after acute treatment with 7, 12-dimethylbenz(a)anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA). Using a two-stage DMBA/TPA carcinogenesis protocol on mouse skin, the number and size of papillomas are increased in RKTG−/− mice, accompanied by shortened tumor latency and enhanced keratinocyte proliferation. The regression of the carcinogen-induced tumors is also prolonged in RKTG−/− mice. Consistently, the levels of Raf-1 and extracellular signal-regulated kinase phosphorylation in primary keratinocytes as well as skin tumors are elevated when RKTG is disrupted. Collectively, our results indicate that RKTG has a suppressive activity in chemical carcinogen-induced mitogenesis and tumor formation in mouse skin.

Journal Article.  3843 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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