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Increased paired box transcription factor 8 has a survival function in Glioma
Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience, Clinical Neuroscience.
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2014 (English)In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 14, 159- p.Article in journal (Refereed) Published
Abstract [en]

Background:

The molecular basis to overcome therapeutic resistance to treat glioblastoma remains unclear. The anti-apoptotic b cell lymphoma 2 (BCL2) gene is associated with treatment resistance, and is transactivated by the paired box transcription factor 8 (PAX8). In earlier studies, we demonstrated that increased PAX8 expression in glioma cell lines was associated with the expression of telomerase. In this current study, we more extensively explored a role for PAX8 in gliomagenesis.

Methods:

PAX8 expression was measured in 156 gliomas including telomerase-negative tumours, those with the alternative lengthening of telomeres (ALT) mechanism or with a non-defined telomere maintenance mechanism (NDTMM), using immunohistochemistry and quantitative PCR. We also tested the affect of PAX8 knockdown using siRNA in cell lines on cell survival and BCL2 expression.

Results:

Seventy-two percent of glioblastomas were PAX8-positive (80% telomerase, 73% NDTMM, and 44% ALT). The majority of the low-grade gliomas and normal brain cells were PAX8-negative. The suppression of PAX8 was associated with a reduction in both cell growth and BCL2, suggesting that a reduction in PAX8 expression would sensitise tumours to cell death.

Conclusions:

PAX8 is increased in the majority of glioblastomas and promoted cell survival. Because PAX8 is absent in normal brain tissue, it may be a promising therapeutic target pathway for treating aggressive gliomas.

Place, publisher, year, edition, pages
2014. Vol. 14, 159- p.
Keyword [en]
PAX8, Glioblastoma, Glioma, Telomere maintenance mechanism, Telomerase, ALT, BCL2, Cell survival
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:umu:diva-88287DOI: 10.1186/1471-2407-14-159ISI: 000333420600003PubMedID: 24602166OAI: oai:DiVA.org:umu-88287DiVA: diva2:715614
Available from: 2014-05-05 Created: 2014-04-29 Last updated: 2017-12-05Bibliographically approved

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