ENO1 and Cancer

Huang, Chen; Sun, Ying; Ping, Yong

doi:10.1016/j.omto.2021.12.026

Cited by 66 publications

(57 citation statements)

References 87 publications

(128 reference statements)

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“…ENO1 (ENO-α), ENO2 (ENO-γ) and ENO3 (ENO-β) are three enolase isoforms in mammalian cells, catalyzing the transformation of 2-PG to PEP during glycolysis. ENO1, also referred to as 2-phospho-D-glycerate hydrolase, is a multifunctional oncoprotein that is present both at the cell surface and in the cytoplasm, contributing to it displaying seven out of ten “hallmarks of cancer” [ 37 , 38 ]. Many studies have demonstrated that the localization and overexpression of ENO1 on the cancer cell surface make it a potential prognostic and diagnostic cancer biomarker as well as an accessible oncotarget [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

Mediation of PKM2-dependent glycolytic and non-glycolytic pathways by ENO2 in head and neck cancer development

Gao

Yang

Tang

et al. 2023

J Exp Clin Cancer Res

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Background Enolase 2 (ENO2) is a crucial glycolytic enzyme in cancer metabolic process and acts as a “moonlighting” protein to play various functions in diverse cellular processes unrelated to glycolysis. ENO2 is highly expressed in head and neck squamous cell carcinoma (HNSCC) tissues relative to normal tissues; however, its impact and underlying regulatory mechanisms in HNSCC malignancy remain unclear. Methods Molecular alterations were examined by bioinformatics, qRT-PCR, western blotting, immunofluorescence, immunohistochemistry, immunoprecipitation, and ChIP-PCR assays. Metabolic changes were assessed by intracellular levels of ATP and glucose. Animal study was used to evaluate the therapeutic efficacy of the ENO inhibitor. Results ENO2 is required for HNSCC cell proliferation and glycolysis, which, surprisingly, is partially achieved by controlling PKM2 protein stability and its nuclear translocation. Mechanistically, loss of ENO2 expression promotes PKM2 protein degradation via the ubiquitin-proteasome pathway and prevents the switch of cytoplasmic PKM2 to the nucleus by inactivating AKT signaling, leading to a blockade in PKM2-mediated glycolytic flux and CCND1-associated cell cycle progression. In addition, treatment with the ENO inhibitor AP-III-a4 significantly induces HNSCC remission in a preclinical mouse model. Conclusion Our work elucidates the signaling basis underlying ENO2-dependent HNSCC development, providing evidence to establish a novel ENO2-targeted therapy for treating HNSCC.

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Section: Discussionmentioning

confidence: 99%

Mediation of PKM2-dependent glycolytic and non-glycolytic pathways by ENO2 in head and neck cancer development

Gao

Yang

Tang

et al. 2023

J Exp Clin Cancer Res

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“…ENO1 overexpression and post-translational modifications were observed to have diagnostic and prognostic value in many cancer types [ 43 ]. ENO1 plays several roles in regard to cancer growth modulation, such as catalyzing glycolysis, maintaining mitochondrial membrane stability, regulating signaling pathways, and reorganizing the cytoskeleton, as well as binding plasminogen when expressed on the surface, a process exploited by cancer cells to promote metastasis, migration, and invasion [ 44 ]. ENO1 has been proposed as a PCa biomarker by numerous proteomics (discussed below in detail), genomics, and functional studies, as well as a biomarker for glioma, neurocytoma, cholangiocarcinoma, lung, kidney, nasopharyngeal cancer, etc.…”

Section: Discussionmentioning

confidence: 99%

Potential Role of Seven Proteomics Tissue Biomarkers for Diagnosis and Prognosis of Prostate Cancer in Urine

Vujicic¹,

Rusevski

Stankov³

et al. 2022

Diagnostics

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As the currently available tests for the clinical management of prostate cancer (PCa) are still far from providing precise diagnosis and risk stratification, the identification of new molecular marker(s) remains a pertinent clinical need. Candidate PCa biomarkers from the published proteomic comparative studies of prostate tissue (2002–2020) were collected and systematically evaluated. AZGP1, MDH2, FABP5, ENO1, GSTP1, GSTM2, and EZR were chosen for further evaluation in the urine of 85 PCa patients and controls using ELISA. Statistically significant differences in protein levels between PCa and BPH showed FABP5 (p = 0.019) and ENO1 (p = 0.015). A biomarker panel based on the combination of FABP5, ENO1, and PSA provided the highest accuracy (AUC = 0.795) for PCa detection. The combination of FABP5, EZR, AZGP1, and MDH2 showed AUC = 0.889 in PCa prognosis, with 85.29% of the samples correctly classified into low and high Gleason score (GS) groups. The addition of PSA to the panel slightly increased the AUC to 0.914. AZGP1, FABP5, and EZR showed significant correlation with GS, stage, and percentage of positive biopsy cores. Although validation using larger patient cohorts will be necessary to establish the credibility of the proposed biomarker panels in a clinical context, this study opens a way for the further testing of more high-quality proteomics biomarkers, which could ultimately add value to the clinical management of PCa.

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“…For example, PKM2, overexpressed in the liver of miR22KO mice, is a well-characterized tumor promotor affecting cancer progression and metastasis by regulating cell migration, angiogenesis, and stemness [ 96 ]. ENO1, in addition to deregulating the bioenergetics of cancer cells, was reported to sustain cell proliferation, to induce resistance to death, and to promote invasion and metastasis, in addition to angiogenesis [ 97 ]. Regarding the lipid metabolism, an upregulation of FABP1 in HCC was shown to stimulate angiogenesis and cancer cell migration [ 98 ], while PLIN2 overexpression is observed in many cancers and is suggested to have a role in tumorigenesis, for example, by favoring adaptation to hypoxia [ 99 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-22 Deficiency Fosters Hepatocellular Carcinoma Development in Fatty Liver

Gjorgjieva

Sousa

et al. 2022

Cells

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MiR-22 is mostly considered as a hepatic tumor-suppressor microRNA based on in vitro analyses. Yet, whether miR-22 exerts a tumor-suppressive function in the liver has not been investigated in vivo. Herein, in silico analyses of miR-22 expression were performed in hepatocellular carcinomas from human patient cohorts and different mouse models. Diethylnitrosamine-induced hepatocellular carcinomas were then investigated in lean and diet-induced obese miR-22-deficient mice. The proteome of liver tissues from miR-22-deficient mice prior to hepatocellular carcinoma development was further analyzed to uncover miR-22 regulated factors that impact hepatocarcinogenesis with miR-22 deficiency. MiR-22 downregulation was consistently observed in hepatocellular carcinomas from all human cohorts and mouse models investigated. The time of appearance of the first tumors was decreased and the number of tumoral foci induced by diethylnitrosamine was significantly increased by miR-22-deficiency in vivo, two features which were further drastically exacerbated with diet-induced obesity. At the molecular level, we provide evidence that the loss of miR-22 significantly affects the energetic metabolism and mitochondrial functions of hepatocytes, and the expression of tumor-promoting factors such as thrombospondin-1. Our study demonstrates that miR-22 acts as a hepatic tumor suppressor in vivo by restraining pro-carcinogenic metabolic deregulations through pleiotropic mechanisms and the overexpression of relevant oncogenes.

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ENO1 and Cancer

Cited by 66 publications

References 87 publications

Mediation of PKM2-dependent glycolytic and non-glycolytic pathways by ENO2 in head and neck cancer development

Mediation of PKM2-dependent glycolytic and non-glycolytic pathways by ENO2 in head and neck cancer development

Potential Role of Seven Proteomics Tissue Biomarkers for Diagnosis and Prognosis of Prostate Cancer in Urine

MiR-22 Deficiency Fosters Hepatocellular Carcinoma Development in Fatty Liver

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