| Literature DB >> 15138850 |
Tomomi Hirata1, Hisaki Nagai1, Kiyoshi Koizumi2, Keiko Okino1, Akima Harada1, Masamitsu Onda1, Takemitsu Nagahata1, Iwao Mikami2, Kyoji Hirai2, Syuji Haraguchi2, Enjing Jin3, Oichi Kawanami3, Kazuo Shimizu2, Mitsuru Emi4.
Abstract
The Ras-CRK-Rap1 cellular signal-transduction system is regulated by guanine nucleotide exchange factors (GEFs). Transcription of C3G on chromosome 9q34 and a key member of the GEF gene family is activated by the CRK-adaptor protein; the C3G product is a CRK SH3 domain-binding guanine nucleotide-releasing factor. We document here the amplification of C3G in five of 18 primary non-small cell lung cancers examined and its increased expression in 18 of 28 tumors in comparison to corresponding non-cancerous lung tissues. Immunohistochemical staining revealed prominent C3G protein in the cytoplasm of cancer cells, associated with faint staining at the nucleolar membrane, but C3G was not detectable in normal bronchial mucoepithelial cells or in broncholoalveolar cells of the bronchial/bronchiolar ducts or alveoli. These data indicate that amplification and increased expression of the C3G gene may play some role in human lung carcinogenesis through derangement of the CRK-Rap1 signaling pathway.Entities:
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Year: 2004 PMID： 15138850 DOI： 10.1007/s10038-004-0148-1
Source DB: PubMed Journal: J Hum Genet ISSN： 1434-5161 Impact factor: 3.172