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CD43 promotes cell growth and helps to evade FAS-mediated apoptosis in non-hematopoietic cancer cells lacking the tumor suppressors p53 or ARF.

Journal article
Authors L Kadaja-Saarepuu
Sirle Laos
K Jääger
J Viil
A Balikova
M Lõoke
Gunnar C. Hansson
Toivo Maimets
Published in Oncogene
Volume 27
Issue 12
Pages 1705-15
ISSN 1476-5594
Publication year 2008
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 1705-15
Language en
Keywords Animals, Antigens, CD43, genetics, physiology, Antigens, CD95, physiology, Apoptosis, genetics, physiology, Cell Line, Tumor, Cell Proliferation, Cyclin-Dependent Kinase Inhibitor p16, deficiency, genetics, physiology, Genes, p53, HCT116 Cells, Humans, Intercellular Signaling Peptides and Proteins, genetics, physiology, Mice, Neoplasms, metabolism, pathology, Signal Transduction, genetics, Tumor Suppressor Protein p53, deficiency
Subject categories Medical and Health Sciences


CD43 is a highly glycosylated transmembrane protein expressed on the surface of most hematopoietic cells. Expression of CD43 has also been demonstrated in many human tumor tissues, including colon adenomas and carcinomas, but not in normal colon epithelium. The potential contribution of CD43 to tumor development is still not understood. Here, we show that overexpression of CD43 increases cell growth and colony formation in mouse and human cells lacking expression of either p53 or ARF (alternative reading frame) tumor-suppressor proteins. In addition, CD43 overexpression also lowers the detection of the FAS death receptor on the cell surface of human cancer cells, and thereby helps to evade FAS-mediated apoptosis. However, when both p53 and ARF proteins are present, CD43 overexpression activates p53 and suppresses colony formation due to induction of apoptosis. These observations suggest CD43 as a potential contributor to tumor development and the functional ARF-p53 pathway is required for the elimination of cells with aberrant CD43 expression.

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