Expression, clinicopathological significance, and prognostic potential of AMPK, p-AMPK, PGC-1α, and TFAM in astrocytomas
Abstract AMP-activated protein kinase (AMPK) is a sensor of energy status that maintains cellular energy homeostasis. Activation of AMPK enhances the expression of proliferator-activated receptor γ coactivator 1α (PGC1-α) and subsequently activates mitochondrial transcription factor A (TFAM) to regu...
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Published in | Journal of neuropathology and experimental neurology Vol. 83; no. 1; pp. 11 - 19 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Oxford University Press
22.12.2023
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Subjects | |
Online Access | Get full text |
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Summary: | Abstract
AMP-activated protein kinase (AMPK) is a sensor of energy status that maintains cellular energy homeostasis. Activation of AMPK enhances the expression of proliferator-activated receptor γ coactivator 1α (PGC1-α) and subsequently activates mitochondrial transcription factor A (TFAM) to regulate mitochondrial oxidative respiratory function. The possible functions of AMPK, p-AMPK, PGC-1α, and TFAM and their interactions in astrocytomas are not known. Here, the levels, clinicopathological characteristics, and prognostic potential of AMPK, p-AMPK, PGC-1α, and TFAM expression levels in astrocytomas were evaluated. The results showed that levels of AMPK, p-AMPK, PGC-1α, and TFAM expression was increased in astrocytomas. Strong correlations were observed between AMPK, p-AMPK, PGC-1α, and TFAM expression in patients with astrocytomas. The analysis indicated that the levels of AMPK, p-AMPK, PGC-1α, and TFAM were associated with the survival. AMPK levels, tumor grade, and age were independent prognostic factors predicting poor outcomes in patients with astrocytoma. Together, these results indicate that these 4 targets may play a crucial role in the progression and prognosis of human astrocytomas and that AMPK may represent a potential therapeutic target. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0022-3069 1554-6578 |
DOI: | 10.1093/jnen/nlad094 |