Full metadata record
DC Field | Value | Language |
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dc.creator | Ezponda, T. (Teresa) | |
dc.creator | Pajares, M.J. (María José) | |
dc.creator | Agorreta, J. (Jackeline) | |
dc.creator | Echeveste, J.I. (José I.) | |
dc.creator | Lopez-Picazo, J.M. (José M.) | |
dc.creator | Torre, W. (Wenceslao) | |
dc.creator | Pio, R. (Rubén) | |
dc.creator | Montuenga-Badia, L.M. (Luis M.) | |
dc.date.accessioned | 2010-09-23T09:19:37Z | - |
dc.date.available | 2010-09-23T09:19:37Z | - |
dc.date.issued | 2010-08-03 | - |
dc.identifier.citation | Ezponda T, Pajares MJ, Agorreta J, Echeveste JI, Lopez-Picazo JM, Torre W, et al. The oncoprotein SF2/ASF promotes non-small cell lung cancer survival by enhancing survivin expression. Clin Cancer Res 2010 Aug 15;16(16):4113-4125. | es_ES |
dc.identifier.issn | 1078-0432 | - |
dc.identifier.uri | https://hdl.handle.net/10171/12900 | - |
dc.description.abstract | Abstract Purpose: SF2/ASF is a splicing factor recently described as an oncoprotein. In the present work, we examined the role of SF2/ASF in human non–small cell lung cancer (NSCLC) and analyzed the molecular mechanisms involved in SF2/ASF-related carcinogenesis. Experimental Design: SF2/ASF protein levels were analyzed in 81 NSCLC patients by immunohistochemistry. SF2/ASF downregulation cellular models were generated using small interfering RNAs, and the effects on proliferation and apoptosis were evaluated. Survivin and SF2/ASF expression in lung tumors was analyzed by Western blot and immunohistochemistry. Survival curves and log-rank test were used to identify the association between the expression of the proteins and time to progression. Results: Overexpression of SF2/ASF was found in most human primary NSCLC tumors. In vitro downregulation of SF2/ASF induced apoptosis in NSCLC cell lines. This effect was associated with a reduction in the expression of survivin, an antiapoptotic protein widely upregulated in cancer. In fact, SF2/ASF specifically bound survivin mRNA and enhanced its translation, via a mammalian target of rapamycin complex 1 (mTORC1) pathway-dependent mechanism, through the phosphorylation and inactivation of the translational repressor 4E-BP1. Moreover, SF2/ASF promoted the stability of survivin mRNA. A strong correlation was observed between the expression of SF2/ASF and survivin in tumor biopsies from NSCLC patients, supporting the concept that survivin expression levels are controlled by SF2/ASF. Furthermore, combined expression of these proteins was associated with prognosis. Conclusion: This study provides novel data on the mTORC1- and survivin-dependent mechanisms of SF2/ASF-related carcinogenic potential, and shows that SF2/ASF and survivin expression is involved in NSCLC progression. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | American Association for Cancer Research | es_ES |
dc.rights | info:eu-repo/semantics/closedAccess | - |
dc.subject | The Oncoprotein SF2/ASF | es_ES |
dc.subject | Promotes Non–Small | es_ES |
dc.subject | Cell Lung Cancer | es_ES |
dc.subject | Survival | es_ES |
dc.subject | Enhancing | es_ES |
dc.subject | Survivin Expression | es_ES |
dc.title | The oncoprotein SF2/ASF promotes non-small cell lung cancer survival by enhancing survivin expression | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.identifier.doi | http://dx.doi.org/10.1158/1078-0432.CCR-10-0076 | es_ES |
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