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 inJournal of neuropathology and experimental neurology Vol. 83; no. 1; pp. 11 - 19
Main Authors Wang, Juan, Lou, Lei, Li, Dan, Wang, Yuan, Jia, Xin, Hao, Xue, Liu, Weina, Li, Yuehong, Wu, Wenxin, Hou, Lianguo, Cui, Jinfeng
Format Journal Article
LanguageEnglish
Published England Oxford University Press 22.12.2023
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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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ISSN:0022-3069
1554-6578
DOI:10.1093/jnen/nlad094