4.5 Article

Overexpression of RGC-32 in colon cancer and other tumors

期刊

EXPERIMENTAL AND MOLECULAR PATHOLOGY
卷 78, 期 2, 页码 116-122

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yexmp.2004.11.001

关键词

RGC-32; colon cancer; cell cycle; Ki-67; cancer

资金

  1. NIEHS NIH HHS [ES 07263] Funding Source: Medline
  2. NINDS NIH HHS [R01 NS42011] Funding Source: Medline

向作者/读者索取更多资源

Tumors often exhibit deregulation of the cell cycle and overexpression of cyclins and cyclin-dependent kinases (CDKs). Response gene to complement (RGC)-32 is a substrate and regulator of CDC2 and its overexpression induces cell cycle activation, We investigated RGC-32 mRNA and protein expression in tumors with special emphasis in colon carcinoma. By using an expression array technique we found that 19% of tumor tissues showed increased RGC-32 mRNA expression over the levels of corresponding normal tissues, On the other hand, an increased RGC-32 protein was found in 70% of colon adenocarcinoma samples tested. In colon carcinomas, two major patterns of RGC-32 immunoreactivity were seen: staining of malignant epithelial cells only in some tumors and RGC-32 reactivity of both malignant epithelia as well as cells in the interstitium in others. Colonic epithelium obtained from normal individuals was consistently negative for RGC-32 protein. Overexpression of RGC-32 protein was found in other tumors including prostate, bladder, breast. lung, and other digestive tract tumors. RGC-32 expression was present in the same malignant epithelial cells that also expressed the proliferation marker Ki-67. Our data suggest that RGC-32 overexpression might be part of the deregulation of the cell cycle that is required for the growth of tumor cells, (c) 2004 Elsevier Inc. All rights reserved.

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