Overexpression of RGC-32 in colon cancer and other tumors

Matthew Fosbrink, Cornelia Cudrici, Florin Niculescu, Tudor C. Badea, Stefan David, Abulkalam Shamsuddin, Moon L. Shin, Horea Rus

Research output: Contribution to journalArticlepeer-review

47 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)116-122
Number of pages7
JournalExperimental and Molecular Pathology
Issue number2
StatePublished - Apr 2005
Externally publishedYes


  • Cancer
  • Cell cycle
  • Colon cancer
  • Ki-67
  • RGC-32

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Clinical Biochemistry


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