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a Istituto Nazionale per lo Studio e la Cura dei Tumori, Via Venezian 1, 20133 Milano, Italy b Istituto di Genetica Molecolare CNR, Via Abbiategrasso 207, 27100 Pavia, Italy
Key Words: c-myc • P-c-Myc • prostate carcinoma • paclitaxel • apoptosis
Address for correspondence: Rosanna Supino, Istituto Nazionale Tumori, Via Venezian 1, 20133 Milano, Italy. Voice: +39-02-23903081; fax: +39-02-23902692. e-mail: rosanna.supino{at}istitutotumori.mi.it
The proto-oncogene c-myc is involved in multiple cell pathways with opposite effects on cell outcome of death or proliferation. It has been proposed that these different roles depend on the sequestration of c-Myc protein in cellular compartments and/or its phosphorylation. We speculated that subcellular localization of c-Myc protein and of its phosphorylated form (P-c-Myc) could have a role in the different response to paclitaxel (PTX) in two prostate carcinoma cell lines, PC3 and DU145, which undergo either multinucleation or c-myc-dependent apoptosis, respectively. c-myc is amplified only in PC3, but a similar extent of c-Myc phosphorylation was observed in both cell lines after PTX treatment. We found that PTX-induced upregulation of c-myc in DU145 cells, not occurring in PC3 cells, cannot be ascribed to a different protein localization, and that a comparable c-Myc and P-c-Myc nuclear translocation occurs in both cell lines after drug treatment. Thus, subcellular localization of c-Myc and P-c-Myc is not crucial in determining the mode of cell death in these prostate carcinoma cell lines.
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