Recommend Cell Cycle to your librarian for 2008. Download form here.

Sign up for Table of Contents Alerts.

home subscribe search archive forthcoming

Email this page Print this page

Extra Views

Myc Overexpression Enhances Apoptosis Induced by Small Molecules

Hao Mo, Marina Vita, Marianne Crespin and Marie Henriksson

volume 5 | issue 19

1 october 2006
Pages: 2191 - 2194

We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.

The Myc oncogene is deregulated in a wide variety of human tumors hence the Myc pathway is regarded as an attractive target for tailored cancer treatment. We have recently identified two small molecules, MYRAs (Myc-pathway response agents), that induce apoptosis in a Myc-dependent manner and inhibit Myc-driven transformation. Here, we show that these compounds in addition have prominent effects in MYCN overexpressing neuroblastoma cells. A third compound, NSC308848, also induced apoptosis in Myc-overexpressing cells and inhibited Myc-induced cellular transformation. However, in contrast to the MYRAs, NSC308848 treatment resulted in decreased Myc protein levels and gave rise to inhibitory effects also on other transcription factors than Myc. Taken together, our findings suggest that these three small molecules can elicit a similar biological response by interfering with the Myc pathway at different levels.

Authors

Hao Mo

Karolinska Institutet

Marina Vita

Karolinska Institutet

Marianne Crespin

Karolinska Institutet

Marie Henriksson

Karolinska Institutet



We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.