Phorbol esters induce death in MCF-7 breast cancer cells with altered expression of protein kinase C isoforms. Role for p53-independent induction of gadd-45 in initiating death.
dc.contributor.author | de Vente, James E. | en_US |
dc.contributor.author | Kukoly, Cynthia A. | en_US |
dc.contributor.author | Bryant, Winifred O. | en_US |
dc.contributor.author | Posekany, Karla J. | en_US |
dc.contributor.author | Chen, Jianming | en_US |
dc.contributor.author | Fletcher, Donald J. | en_US |
dc.contributor.author | Parker, Peter J. | en_US |
dc.contributor.author | Pettit, George J. | en_US |
dc.contributor.author | Lozano, Guillermina | en_US |
dc.contributor.author | Cook, Paul P. | en_US |
dc.contributor.author | Ways, D. Kirk | en_US |
dc.date.accessioned | 2011-02-17T16:48:34Z | en_US |
dc.date.accessioned | 2011-05-17T00:25:40Z | |
dc.date.available | 2011-02-17T16:48:34Z | en_US |
dc.date.available | 2011-05-17T00:25:40Z | |
dc.date.issued | 1995-10 | en_US |
dc.description.abstract | Protein kinase C (PKC) modulates growth, differentiation, and apoptosis in a cell-specific fashion. Overexpression of PKC-a in MCF-7 breast cancer cells (MCF-7-PKC-a cell) leads to expression of a more transformed phenotype. The response of MCF-7 and MCF-7-PKC-c cells to phorbol esters (TPA) was examined. TPA-treated MCF-7 cells demonstrated a modest cytostatic response associated with a G, arrest that was accompanied by Cipl expression and retinoblastoma hypophosphorylation. While p53 was detected in MCF-7 cells, evidence for TPA-induced stimulation of p53 transcriptional activity was not evident. In contrast, TPA treatment induced death of MCF-7-PKC-a cells. Bryostatin 1, another PKC activator, exerted modest cytostatic effects on MCF-7 cells while producing a cytotoxic response at low doses in MCF-7-PKC-a cells that waned at higher concentrations. TPA-treated MCF-7-PKC-a cells accumulated in G2/M, did not express p53, displayed decreased Cipl expression, and demonstrated a reduction in retinoblastoma hypophosphorylation. TPA-treated MCF-7-PKC-a cells expressed gadd45 which occurred before the onset of apoptosis. Thus, alterations in the PKC pathway can modulate the decision of a breast cancer cell to undergo death or differentiation. In addition, these data show that PKC activation can induce expression ofgadd45 in a p53-independent fashion. Originally published Journal of Clinical Investigation, Vol. 96, No. 4, Oct 1995 | en_US |
dc.identifier.citation | Journal of Clinical Investigation; 96:4 p. 1874-1886 | en_US |
dc.identifier.pmid | PMC185824 | en_US |
dc.identifier.uri | http://hdl.handle.net/10342/3254 | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | East Carolina University | en_US |
dc.relation.uri | http://www.jci.org/archive | en_US |
dc.rights | Author notified of opt-out rights by Cammie Jennings prior to upload of this article. | en_US |
dc.subject | Protein kinase C | en_US |
dc.subject | Phorbol esters | en_US |
dc.subject | Breast--Cancer | en_US |
dc.subject | Apoptosis | en_US |
dc.subject | p53 | en_US |
dc.title | Phorbol esters induce death in MCF-7 breast cancer cells with altered expression of protein kinase C isoforms. Role for p53-independent induction of gadd-45 in initiating death. | en_US |
dc.type | Article | en_US |
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