Please use this identifier to cite or link to this item: https://doi.org/10.1002/mc.10082
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dc.titleInduction of marked apoptosis in mammalian cancer cell lines by antisense DNA treatment to abolish expression of DENN (Differentially Expressed in Normal and Neoplastic Cells)
dc.contributor.authorLim, K.M.
dc.contributor.authorChow, V.T.K.
dc.date.accessioned2016-11-28T10:20:47Z
dc.date.available2016-11-28T10:20:47Z
dc.date.issued2002-11-01
dc.identifier.citationLim, K.M., Chow, V.T.K. (2002-11-01). Induction of marked apoptosis in mammalian cancer cell lines by antisense DNA treatment to abolish expression of DENN (Differentially Expressed in Normal and Neoplastic Cells). Molecular Carcinogenesis 35 (3) : 110-126. ScholarBank@NUS Repository. https://doi.org/10.1002/mc.10082
dc.identifier.issn08991987
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/131484
dc.description.abstractWe previously reported the isolation of the novel human DENN gene, which is differentially expressed in normal and neoplastic cells. DENN is identical to MADD (mitogen-activated protein kinase-activating death domain), which interacts with tumor necrosis factor receptor 1 through their death domains. DENN is also homologous to Rab3 GEP, a rat Rab3 GDP/GTP exchange protein. Real-time reverse transcription -polymerase chain reaction analysis showed that DENN expression in cancer cell lines was 26-50 times that in normal cells. The Jurkat human leukemia, PLC/PRF/5 human hepatoma, and NS-1 mouse myeloma cell lines as well as the MRC-5 human fetal lung and Vero monkey kidney cell lines were treated successfully with four separate DENN-targeted antisense oligodeoxynucleotides (ODNs) to abrogate DENN expression. Quantitative assessment of cell viability and apoptosis by flow cytometry via fluorescein diacetate and propidium iodide membrane-integrity tests, terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate-biotin nick end-labeling, and annexin V assays showed that antisense silencing of DENN resulted in markedly more pronounced cell death in cancer cells compared with nonmalignant cells. Antisense-treated cell lines exhibited extensive loss of DNA content, forming distinct sub-G1 peaks, while cell proliferation diminished significantly. Ultrastructural features of programmed cell death in cells subjected to antisense ODNs were authenticated by electron microscopy. In contrast, transfection of cell lines with a plasmid construct to achieve DENN overexpression augmented cellular proliferation and could reverse the apoptotic effect of antisense and staurosporine treatment. Our findings suggest that DENN is intimately involved in anti-apoptotic and cell-survival processes. © 2002 Wiley-Liss, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1002/mc.10082
dc.sourceScopus
dc.subjectAntisense
dc.subjectApoptosis
dc.subjectDeath domain
dc.subjectDENN
dc.subjectMADD
dc.typeArticle
dc.contributor.departmentBIOPROCESSING TECHNOLOGY CENTRE
dc.contributor.departmentMICROBIOLOGY
dc.description.doi10.1002/mc.10082
dc.description.sourcetitleMolecular Carcinogenesis
dc.description.volume35
dc.description.issue3
dc.description.page110-126
dc.description.codenMOCAE
dc.identifier.isiut000179030800002
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