2005
DOI: 10.1158/1078-0432.ccr-04-2071
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Disruption of Cooperation Between Ras and MycN in Human Neuroblastoma Cells Promotes Growth Arrest

Abstract: Purpose: Our aim was to examine whether active Ras and MycN cooperation contributes to the malignant phenotype of humanneuroblastoma with amplified MycN gene, an aggressive incurable tumor. Experimental Design: Human neuroblastoma LAN-1 cells, in which the MycN gene is amplified, were used to examine the impact of the Ras inhibitor farnesylthiosalicylic acid on cell growth, on the levels Ras and MycN proteins, and on profiles of gene expression. Results: We show that LAN-1 cells express relatively large amount… Show more

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Cited by 58 publications
(65 citation statements)
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“…Rapamycin treatment induced a G 1 arrest whereas CCI-779 induced cell cycle arrest in the S and G 2 phase (Table 3). The observed S/G 2 arrest may be due to repression of MYCN since MYCN has been shown to activate expression of S-phase specific cyclins, with cyclin D1 being one of the major mediators (Yaari et al, 2005). We also noticed that only a minor fraction of SK-N-AS cells treated with rapamycin had sub-G 1 DNA content.…”
Section: Sh-sy5y Sk-n-asmentioning
confidence: 63%
“…Rapamycin treatment induced a G 1 arrest whereas CCI-779 induced cell cycle arrest in the S and G 2 phase (Table 3). The observed S/G 2 arrest may be due to repression of MYCN since MYCN has been shown to activate expression of S-phase specific cyclins, with cyclin D1 being one of the major mediators (Yaari et al, 2005). We also noticed that only a minor fraction of SK-N-AS cells treated with rapamycin had sub-G 1 DNA content.…”
Section: Sh-sy5y Sk-n-asmentioning
confidence: 63%
“…Recent reports indicate that activation of the PI3K-Akt-signaling pathway is involved in neuroblastoma progression, and its activation also predicts poor prognosis in primary neuroblastoma (Yaari et al, 2005;Chesler et al, 2006;Ishola et al, 2007;Opel et al, 2007;Kang et al, 2008). In addition, PI3K-Akt induces stabilization of MYCN protein (Yaari et al, 2005;Chesler et al, 2006). Our earlier report documented that AEG-1 activates cell survival through activation of the PI3K-Akt-signaling pathway (Lee et al, 2008b).…”
Section: Discussionmentioning
confidence: 79%
“…Role of the PI3K-Akt-signaling pathway and MYCN in AEG-1-mediated neuroblastoma progression Recent studies suggest that the PI3K-Akt-signaling pathway is involved in tumor progression and poor outcome of neuroblastoma and contributes to the stabilization of the MYCN protein (Yaari et al, 2005;Chesler et al, 2006;Opel et al, 2007). Our earlier investigations documented that AEG-1 activates cell survival through the PI3K-Akt-signaling pathway (Lee et al, 2008b).…”
Section: Overexpression Of Aeg-1 In Tet21n Cells Enhances Expressionmentioning
confidence: 85%
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“…Expression of Nmyc in nonamplified neuroblastoma cell lines can induce reentry of quiescent cells into the cell cycle and correlates with growth rate, motility, and cell attachment (42). The driving oncogenic role of N-myc is also enhanced by cooperating events such as RAS mutation due to Ras-mediated stabilization of N-myc and/or increase in N-myc translation (40,43,44). High expression of N-myc is associated with proliferation and induction of cell-cycle genes (45,46) and also plays a role in regulation of apoptotic cell death (47).…”
Section: Functional Targets Of N-mycmentioning
confidence: 99%