AMPK-dependent phosphorylation of HDAC8 triggers PGM1 expression to promote lung cancer cell survival under glucose starvation

Li, Yanping; Liang, Ronghui; Sun, Mingming; Li, Zhen; Sheng, Hao; Wang, Jiyan; Xu, Pengjuan; Liu, Shuangping; Yang, Wancai; Lü, Bin; Zhang, Shuai; Shan, Changliang

doi:10.1016/j.canlet.2020.03.007

Cited by 41 publications

(32 citation statements)

References 21 publications

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“…Existing studies support these results. For example, PGM1 has been downregulated in lung cancer cells and hepatic cancer cells [6,7,17]. PGM5 is a downregulated tumour suppressor gene in colorectal cancer, suggesting that PGM5 has the potential to be a new predictor and treatment target for colorectal cancer [10].…”

Section: Discussionmentioning

confidence: 99%

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A Wide-angle Glance Of Phosphoglucomutase Gene Family In Pan-Cancer

Liu

Shen

et al. 2021

Preprint

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Background Phosphoglucomutases (PGMs) are a group of important enzymes in glucose metabolism. The PGM family play roles in a variety of cancers, but we still lack a comprehensive understanding of the relationship between the PGM family and pan-cancer. Methods We extracted data from the Cancer Genome Atlas, Oncomine, Human Protein Atlas, and Cancer Cell Line Encyclopedia databases. The R language was mainly used for analysis. Results The PGM1 and PGM5 genes both show low expression in breast cancer, colon cancer, and hepatocellular carcinoma. The expression of PGMs is related to signal transduction pathways, such as protein secretion, ultraviolet (UV) response, and DNA repair pathways, and the infiltration of immune cells such as naive B cells, activated natural killer cells, and resting mast cells in cancers. PGM5 is associated with a higher survival rate in clear-cell renal carcinoma and cervical cancer and a lower survival rate in squamous-cell lung cancer and hepatocellular carcinoma. The copy number variation of PGMs have a broad impact on their expression. In breast cancer, colon cancer, and other cancers, PGM1 is upregulated when it has a higher copy number. Genetic variations in PGMs have adverse effects on the prognosis of various types of cancers. PGM5 mutations in liver cancer and sarcoma and PGM1 copy number deletion in cholangiocarcinoma are all risk factors for those cancers. The qRT-PCR experiments verified the higher expression of PGM2L1 and the lower expression of PGM5 in gastric cancer, and the lower expression of PGM1 and PGM5 in colorectal cancer. Conclusion The expression of PGMs is heterogeneous in cancer tissues and is associated with cancer activation pathways as well as immune cell infiltration. The expression of PGMs can affect the prognosis of a variety of cancers. Mutation or copy number variation of PGMs will affect their expression in cancers, as well as the cancer prognosis. These findings provide a foundation for investigating the role of PGMs in the prediction/diagnosis/prognosis of cancers and provide new clues for finding targets for cancer treatment.

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Section: Discussionmentioning

confidence: 99%

“…They had been reported that PGM1 can inhibit the progression of hepatic carcinoma by controlling glucose transport [6]. PGM1 is highly expressed in lung cancer tissue and is associated with its poor prognosis [7]. PGM3 is associated with breast cancer.…”

Section: Introductionmentioning

confidence: 99%

A Wide-angle Glance Of Phosphoglucomutase Gene Family In Pan-Cancer

Liu

Shen

et al. 2021

Preprint

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“…Once competed for resources become low, the deprivation of glucose reverses glycolysis and consequently elevates the enzyme PGM as well as the enzymes at each step in the catabolic conversion of glycogen to glucose and ultimately to lactate and ROS. Aberrations in the abundance of enzymes involved in glycogen metabolism, particularly during glucose deprivation, have been noted for a number of cancers [ 42 , 43 ] and are associated with elevated levels of PGM, premature senescence [ 44 ], cancer cell survival and poor prognosis [ 42 ]. Elevation of the PGM protein with increased activity of the PGM late into PM time, along with the increase in other glycolytic enzymes, demonstrates a drive toward lactate production after death.…”

Section: Discussionmentioning

confidence: 99%

The Molecular Floodgates of Stress-Induced Senescence Reveal Translation, Signalling and Protein Activity Central to the Post-Mortem Proteome

Wasinger

Curnoe

Boel

et al. 2020

IJMS

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The transitioning of cells during the systemic demise of an organism is poorly understood. Here, we present evidence that organismal death is accompanied by a common and sequential molecular flood of stress-induced events that propagate the senescence phenotype, and this phenotype is preserved in the proteome after death. We demonstrate activation of “death” pathways involvement in diseases of ageing, with biochemical mechanisms mapping onto neurological damage, embryonic development, the inflammatory response, cardiac disease and ultimately cancer with increased significance. There is sufficient bioavailability of the building blocks required to support the continued translation, energy, and functional catalytic activity of proteins. Significant abundance changes occur in 1258 proteins across 1 to 720 h post-mortem of the 12-week-old mouse mandible. Protein abundance increases concord with enzyme activity, while mitochondrial dysfunction is evident with metabolic reprogramming. This study reveals differences in protein abundances which are akin to states of stress-induced premature senescence (SIPS). The control of these pathways is significant for a large number of biological scenarios. Understanding how these pathways function during the process of cellular death holds promise in generating novel solutions capable of overcoming disease complications, maintaining organ transplant viability and could influence the findings of proteomics through “deep-time” of individuals with no historically recorded cause of death.

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“…It may be a novel angle to elucidate the pathogenesis of SCCHN from the perspective of miR-223-3p regulating the EMT. Analyses also suggested that miR-223-3p and miR-204-5p may affect the energy balance of SCCHN through AMPK signaling pathway, a proved regulatory signaling pathway for the energy metabolism of tumors [44][45][46][47]. Energy metabolism plays important roles in cancer progression and the regulation of energy metabolism balance may become one of the effective anti-tumor treatment methods [48,49].…”

Section: Discussionmentioning

confidence: 99%

Clinical significance and potential mechanisms of miR-223-3p and miR-204-5p in squamous cell carcinoma of head and neck: a study based on TCGA and GEO

et al. 2020

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ObjectiveTo explore the clinical significance and mechanisms of altered miRNAs in squamous cell carcinoma of head and neck (SCCHN) and provide references for SCCHN diagnosis and prognosis.MethodDifferential expressed miRNAs (DEMs) in SCCHN were screened through gene expression omnibus (GEO) DataSets and verified by the cancer genome atlas (TCGA) database. Next, the overall survival analysis, receiver operating characteristics, and clinical correlation analysis were adopted to filter the miRNAs with diagnostic and prognostic values. Finally, functional enrichment analyses were conducted for inquiring into the mechanisms of miRNAs.ResultsTotal 103 DEMs (p < 0.05, fold change ≥ 2) in SCCHN were screened out from GSE124566. Partly, the expression levels of the selected (12/17) miRNAs were verified by TCGA. Followed, of the 12 miRNAs, two miRNA expression levels were associated with the overall survival, and five miRNAs showed diagnostic values (AUC ≥ 0.85). Besides, miR-223-3p and miR-204-5p expression levels were correlated to certain clinical features. Epithelial–mesenchymal transition (EMT) related biological process and energy metabolism controlling related AMPK signaling pathway might mediate the roles of miR-223-3p and miR-204-5p, respectively.ConclusionWith diagnostic and prognostic values, miR-223-3p and miR-204-5p may be involved in the progression of SCCHN through EMT-related biological process and energy balance related AMPK signaling pathway, respectively.

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AMPK-dependent phosphorylation of HDAC8 triggers PGM1 expression to promote lung cancer cell survival under glucose starvation

Cited by 41 publications

References 21 publications

A Wide-angle Glance Of Phosphoglucomutase Gene Family In Pan-Cancer

A Wide-angle Glance Of Phosphoglucomutase Gene Family In Pan-Cancer

The Molecular Floodgates of Stress-Induced Senescence Reveal Translation, Signalling and Protein Activity Central to the Post-Mortem Proteome

Clinical significance and potential mechanisms of miR-223-3p and miR-204-5p in squamous cell carcinoma of head and neck: a study based on TCGA and GEO

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