The tyrosine kinase Src is frequently activated in advanced human prostate carcinomas and its activation correlates with tyrosine phosphorylation of the RNA-binding protein Sam68. Herein, we have investigated the expression and function of Sam68 in human prostate cancer cells. Analysis of specimens obtained from 20 patients revealed that Sam68 is upregulated at the protein level in 35% of the samples. Real-time polymerase chain reaction confirmed the results at the mRNA level in most patients. Downregulation of Sam68 by RNAi in LNCaP prostate cancer cells delayed cell cycle progression and reduced the proliferation rate. Moreover, depletion of Sam68 sensitized cells to apoptosis induced by DNA-damaging agents. Similarly, stable cell lines expressing a truncated GFP-Sam68GSG protein displayed reduced growth rates and higher sensitivity to cisplatin-induced apoptosis. Microarray analyses revealed that a subset of genes involved in proliferation and apoptosis were altered when Sam68 was knocked down in LNCaP cells. Our results indicate that Sam68 expression supports prostate cancer cells proliferation and survival to cytotoxic agents. © 2007 Nature Publishing Group All rights reserved.

Busà, R., Paronetto, M.P., Farini, D., Pierantozzi, E., Botti, F., Angelini, D.F., et al. (2007). The RNA-binding protein Sam68 contributes to proliferation and survival of human prostate cancer cells. ONCOGENE, 26(30), 4372-4382 [10.1038/sj.onc.1210224].

The RNA-binding protein Sam68 contributes to proliferation and survival of human prostate cancer cells

Pierantozzi, E.;Sette, C.
2007-01-01

Abstract

The tyrosine kinase Src is frequently activated in advanced human prostate carcinomas and its activation correlates with tyrosine phosphorylation of the RNA-binding protein Sam68. Herein, we have investigated the expression and function of Sam68 in human prostate cancer cells. Analysis of specimens obtained from 20 patients revealed that Sam68 is upregulated at the protein level in 35% of the samples. Real-time polymerase chain reaction confirmed the results at the mRNA level in most patients. Downregulation of Sam68 by RNAi in LNCaP prostate cancer cells delayed cell cycle progression and reduced the proliferation rate. Moreover, depletion of Sam68 sensitized cells to apoptosis induced by DNA-damaging agents. Similarly, stable cell lines expressing a truncated GFP-Sam68GSG protein displayed reduced growth rates and higher sensitivity to cisplatin-induced apoptosis. Microarray analyses revealed that a subset of genes involved in proliferation and apoptosis were altered when Sam68 was knocked down in LNCaP cells. Our results indicate that Sam68 expression supports prostate cancer cells proliferation and survival to cytotoxic agents. © 2007 Nature Publishing Group All rights reserved.
2007
Busà, R., Paronetto, M.P., Farini, D., Pierantozzi, E., Botti, F., Angelini, D.F., et al. (2007). The RNA-binding protein Sam68 contributes to proliferation and survival of human prostate cancer cells. ONCOGENE, 26(30), 4372-4382 [10.1038/sj.onc.1210224].
File in questo prodotto:
File Dimensione Formato  
The RNA-binding protein Sam68.pdf

non disponibili

Tipologia: PDF editoriale
Licenza: NON PUBBLICO - Accesso privato/ristretto
Dimensione 349.78 kB
Formato Adobe PDF
349.78 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/1070805