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High expression of MKP1/DUSP1 counteracts glioma stem cell activity and mediates HDAC inhibitor response
- Arrizabalaga, O. (author)
- Moreno-Cugnon, L. (author)
- Auzmendi-Iriarte, J. (author)
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- Aldaz, P. (author)
- de Caceres,, II (author)
- Garros-Regulez, L. (author)
- Moncho-Amor, V. (author)
- Torres-Bayona, S. (author)
- Pernia, O. (author)
- Pintado-Berninches, L. (author)
- Carrasco-Ramirez, P. (author)
- Cortes-Sempere, M. (author)
- Rosas, R. (author)
- Sanchez-Gomez, P. (author)
- Ruiz, I. (author)
- Pollard, S. (author)
- Garcia, I. (author)
- Sacido, A. A. (author)
- Lovell-Badge, R. (author)
- Belda-Iniesta, C. (author)
- Sampron, N. (author)
- Perona, R. (author)
- Matheu, A. (author)
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- (creator_code:org_t)
- 2017-12-14
- 2017
- English.
- In: Oncogenesis. - : Springer Science and Business Media LLC. - 2157-9024. ; 6
- Journal article (peer-reviewed)
Abstract
Subject headings
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- The elucidation of mechanisms involved in resistance to therapies is essential to improve the survival of patients with malignant gliomas. A major feature possessed by glioma cells that may aid their ability to survive therapy and reconstitute tumors is the capacity for self-renewal. We show here that glioma stem cells (GSCs) express low levels of MKP1, a dual-specificity phosphatase, which acts as a negative inhibitor of JNK, ERK1/2, and p38 MAPK, while induction of high levels of MKP1 expression are associated with differentiation of GSC. Notably, we find that high levels of MKP1 correlate with a subset of glioblastoma patients with better prognosis and overall increased survival. Gain of expression studies demonstrated that elevated MKP1 impairs self-renewal and induces differentiation of GSCs while reducing tumorigenesis in vivo. Moreover, we identified that MKP1 is epigenetically regulated and that it mediates the anti-tumor activity of histone deacetylase inhibitors (HDACIs) alone or in combination with temozolomide. In summary, this study identifies MKP1 as a key modulator of the interplay between GSC self-renewal and differentiation and provides evidence that the activation of MKP1, through epigenetic regulation, might be a novel therapeutic strategy to overcome therapy resistance in glioblastoma.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cancer and Oncology (hsv//eng)
Keyword
- protein-kinase phosphatase-1
- tumor-initiating cells
- human
- breast-cancer
- n-terminal kinase
- p38 mapk
- temozolomide resistance
- human glioblastoma
- pivotal role
- lung-cancer
- activation
- Oncology
Publication and Content Type
- ref (subject category)
- art (subject category)
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- Arrizabalaga, O.
- Moreno-Cugnon, L ...
- Auzmendi-Iriarte ...
- Aldaz, P.
- de Caceres,, II
- Garros-Regulez, ...
- show more...
- Moncho-Amor, V.
- Torres-Bayona, S ...
- Pernia, O.
- Pintado-Berninch ...
- Carrasco-Ramirez ...
- Cortes-Sempere, ...
- Rosas, R.
- Sanchez-Gomez, P ...
- Ruiz, I.
- Carén, Helena, 1 ...
- Pollard, S.
- Garcia, I.
- Sacido, A. A.
- Lovell-Badge, R.
- Belda-Iniesta, C ...
- Sampron, N.
- Perona, R.
- Matheu, A.
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- MEDICAL AND HEALTH SCIENCES
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- Oncogenesis
- By the university
- University of Gothenburg
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