Genes of glycolysis are ubiquitously overexpressed in 24 cancer classes

Altenberg, Brigitte; Greulich, Karl Otto

doi:10.1016/j.ygeno.2004.08.010

Cited by 597 publications

(504 citation statements)

References 7 publications

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“…PKM2 is one of the most highly expressed genes and plays a crucial role in malignant transformation and tumor glucose metabolism. The tumor cells exclusively express PKM2 (27) and upregulation of PKM2 has been found in a few types of tumors (8)(9)(10), including CRC although with lower sample numbers (28). Here, we demonstrated that PKM2 is upregulated in colon cancer tissues compared with normal mucosa (Fig.…”

Section: Discussionsupporting

confidence: 55%

“…However, how cancer cells establish this special metabolism is unclear. Overexpression of glycolytic genes is found to play critical roles in the establishment of tumor aerobic glycolysis (8). PKM2 is one of the most highly expressed genes and plays a crucial role in malignant transformation and tumor glucose metabolism.…”

Section: Discussionmentioning

confidence: 99%

“…Cellular oxygen consumption rates were measured using a water-jacketed (37 8C) anaerobic chamber fitted with a polarographic oxygen electrode as described previously (8). The electrode was calibrated with 150 mM NaCl equilibrated to room air at 37 8C (corresponding to 199 nmol O 2 per ml).…”

Section: Measurement Of Oxygen Consumptionmentioning

confidence: 99%

“…Recent results show that upregulation of glycolytic enzymes plays a crucial role in cancer. Among these enzymes, pyruvate kinase type M2 (PKM2) comprises one of the most unregulated genes in cancers (8)(9)(10). It is shown that expression of PKM2 in cancer cells is essential for the establishment of aerobic glycolysis and provides a selective growth advantage for tumor cells in vivo (10).…”

Section: Introductionmentioning

confidence: 99%

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Pyruvate kinase type M2 is upregulated in colorectal cancer and promotes proliferation and migration of colon cancer cells

Zhou

Sun

et al. 2012

IUBMB Life

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SummaryPyruvate kinase type M2 (PKM2) has been reported to be involved in aerobic glycolysis and cell growth in various tumors. However, the expression pattern of PKM2 in colorectal cancer (CRC) and the correlation between PKM2 expression and CRC remains unclear. The aim of this study is to investigate PKM2 expression and its possible role in CRC. We found that expression of PKM2 was increased in CRC and the increased PKM2 expression was associated with later stage and lymph metastasis of the tumors. Knockdown of PKM2 suppressed the aerobic glycolysis and decreased lactate production of colon cancer RKO cells. Knockdown of PKM2 repressed proliferation and migration of the cells. Inhibition of PKM2 suppressed xenograft tumor growth of RKO cells in vivo. These results suggest that the expression of PKM2 plays a critical role in development of CRC, and it may provide a growth advantage for colon cancer cells. Thus, PKM2 might be a potential therapeutic target for CRC.2012 IUBMB IUBMB Life, 64(9): 775-782, 2012

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Section: Measurement Of Oxygen Consumptionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pyruvate kinase type M2 is upregulated in colorectal cancer and promotes proliferation and migration of colon cancer cells

Zhou

Sun

et al. 2012

IUBMB Life

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“…Pyruvate kinase (PK) regulates the final rate‐limiting step of glycolysis and catalyses the transfer of a phosphate group from phosphoenolpyruvate (PEP) to adenosine diphosphate 14. This transfer yields one molecule each of pyruvate and adenosine triphosphate 15, 16. PKM1, PKM2, PKL and PKR are PK isoforms expressed in different types of mammalian cells and tissues.…”

Section: Introductionmentioning

confidence: 99%

Down‐regulation of PKM2 enhances anticancer efficiency of THP on bladder cancer

Tao

Tang

et al. 2018

J Cellular Molecular Medi

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Pyruvate kinase M2 (PKM2) regulates the final step of glycolysis levels that are correlated with the sensitivity of anticancer chemotherapeutic drugs. THP is one of the major drugs used in non‐muscle‐invasive bladder cancer instillation chemotherapy. However, low response ratio of THP (19.7%) treatment to human genitourinary tumours using collagen gel matrix has been observed. This study aims to investigate the effect of down‐regulation of PKM2 on THP efficiency. Via inhibitor or siRNA, the effects of reduced PKM2 on the efficiency of THP were determined in 2 human and 1 murine bladder cancer cell lines, using MTT, cologenic and fluorescence approaches. Molecular mechanisms of PKM2 on THP sensitization were explored by probing p‐AMPK and p‐STAT3 levels via WB. Syngeneic orthotopic bladder tumour model was applied to evaluate this efficiency in vivo, analysed by Kaplan‐Meier survival curves, body and bladder weights plus immunohistochemistric tumour biomarkers. PKM2 was overexpressed in bladder cancer cells and tissues, and down‐regulation of PKM2 enhanced the sensitivity of THP in vitro. Activation of AMPK is essential for THP to exert anti‐bladder cancer activities. On the other hand, down‐regulating PKM2 activates AMPK and inhibits STAT3, correlated with THP sensitivity. Compared with THP alone (400 μmol L−1, 50 μL), the combination with metformin (60 mmol L−1, 50 μL) stopped growth of bladder cancer completely in vivo (combination group VS normal group P = .078). Down‐regulating the expression of PKM2 enhances the anticancer efficiency of THP. This study provides a new insight for improving the chemotherapeutic effect of THP.

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A 17 gene panel for non‐small‐cell lung cancer prognosis identified through integrative epigenomic‐transcriptomic analyses of hypoxia‐induced epithelial–mesenchymal transition

Chen

Zhang

Wang³

et al. 2019

Molecular Oncology

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As a critical feature of the tumor microenvironment, hypoxia is known to be a potent inducer of tumor metastasis, and it has been proposed that the initial steps in metastasis involve epithelial–mesenchymal transition ( EMT ). The strong correlation among hypoxia, EMT , and metastasis suggests that integrative assessment of gene expression and the DNA modification program of hypoxia‐induced EMT via high‐throughput sequencing technologies may increase our understanding of the molecular basis of tumor invasion and metastasis. Here, we present the genomewide transcriptional and epigenetic profiles of non‐small‐cell lung cancer ( NSCLC ) cells under normoxic and hypoxic conditions. We demonstrate that hypoxia induces EMT along with dynamic alterations of transcriptional expression and epigenetic modifications in both A549 and HCC 827 cells. After training using a dataset from patients with invasive and noninvasive lung adenocarcinomas with an artificial neural network algorithm, a characteristic 17‐gene panel was identified, consisting of genes involved in EMT , hypoxia response, glycometabolism, and epigenetic modifications. This 17‐gene signature clearly stratified NSCLC patients with significant differences in overall survival across three independent datasets. Our study may be suitable as a basis for further selection of gene signatures to potentially guide prognostic stratification in patients with NSCLC .

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Genes of glycolysis are ubiquitously overexpressed in 24 cancer classes

Cited by 597 publications

References 7 publications

Pyruvate kinase type M2 is upregulated in colorectal cancer and promotes proliferation and migration of colon cancer cells

Pyruvate kinase type M2 is upregulated in colorectal cancer and promotes proliferation and migration of colon cancer cells

Down‐regulation of PKM2 enhances anticancer efficiency of THP on bladder cancer

A 17 gene panel for non‐small‐cell lung cancer prognosis identified through integrative epigenomic‐transcriptomic analyses of hypoxia‐induced epithelial–mesenchymal transition

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