ENO1 promotes PDAC progression by inhibiting CD8+ T cell infiltration through upregulating PD-L1 expression via HIF-1α signaling

Translational Oncology, Год журнала: 2025, Номер 52, С. 102261 - 102261

Опубликована: Янв. 5, 2025

Язык: Английский

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ENO2-Regulated Glycolysis in Endothelial Cells Contributes to FGF2-Induced Retinal Neovascularization

Investigative Ophthalmology & Visual Science, Год журнала: 2025, Номер 66(1), С. 58 - 58

Опубликована: Янв. 24, 2025

Purpose: Ocular neovascularization is a major cause of blindness. Although fibroblast growth factor-2 (FGF2) has been implicated in the pathophysiology angiogenesis, underlying mechanisms remain incompletely understood. The purpose this study was to investigate role FGF2 retinal and elucidate its mechanisms. Methods: oxygen-induced retinopathy mouse model used pathogenesis neovascularization. Immunofluorescence quantify retina. Data-independent acquisition proteomics were performed differentially expressed proteins human microvascular endothelial cells stimulated with associated pathways analyzed. We carried out qRT-PCR Western Blot assays detect expression genes at mRNA protein levels. angiogenesis abilities measured by transwell, EdU tube formation assays. Results: significantly upregulated tissues it markedly enhanced formation, migration, proliferation vitro. proteomic analysis identified 287 response stimulation, characterized notable upregulation glycolysis pathway, among which we confirmed that enolase 2 (ENO2) levels elevated after knockdown resulted diminished glycolytic activity impaired angiogenic processes. Furthermore, use ENO2 inhibitor AP-Ⅲ-a4 alleviated vivo Conclusions: Our findings underscore pivotal ENO2-mediated FGF2-induced suggesting may serve as promising therapeutic target for managing pathological

Язык: Английский

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Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections

Open Biology, Год журнала: 2025, Номер 15(2)

Опубликована: Фев. 1, 2025

Glycolysis, present in most organisms, is evolutionarily one of the oldest metabolic pathways. It has great relevance at a physiological level because it responsible for generating ATP cell through conversion glucose into pyruvate and reducing nicotinamide adenine dinucleotide (NADH) (that may be fed electron chain mitochondria to produce additional by oxidative phosphorylation), as well producing intermediates that can serve substrates other processes. Glycolysis takes place 10 consecutive chemical reactions, each which catalysed specific enzyme. Although energy transduction metabolism main function this pathway, involvement virulence, growth, pathogen–host interactions, immunomodulation adaptation environmental conditions are functions attributed pathway. In humans, where glycolysis occurs mainly cytosol, mislocalization some glycolytic enzymes various subcellular locations, alterations their expression regulation, been associated with development progression diseases. review, we describe role pathogenesis diseases clinical interest. addition, potential these targets drug use diagnostic prognostic markers pathologies also discussed.

Язык: Английский

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Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism

Cell Death Discovery, Год журнала: 2025, Номер 11(1)

Опубликована: Март 8, 2025

Abstract Thyroid hormones (THs) dysfunctions have been demonstrated to be associated with the risk of developing different types cancers. The role THs in regulating hepatocellular carcinoma (HCC) progression is still controversial. We that T3 can inhibit HCC by enhancing expression THRSP. Mechanistically, activate tumor suppressor LKB1/AMPK/Raptor signaling as well oncogenic PI3K/Akt HCC. Interestingly, T3-induced THRSP augment activation signaling, yet activation, thereby preventing mTOR-induced nuclear translocation HIF-1α, and ultimately suppressing ENO2-induced glycolysis progression. More importantly, exogenous enhances antitumor effect multikinase inhibitor lenvatinib vitro vivo glycolysis. Our findings reveal mechanism glucose metabolism provide new potential therapeutic strategies for treatment drug resistance reversal.

Язык: Английский

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Deletion of ENO1 sensitizes pancreatic cancer cells to gemcitabine via MYC/RRM1-mediated glycolysis

Scientific Reports, Год журнала: 2025, Номер 15(1)

Опубликована: Март 22, 2025

Glycolysis is a critical metabolic pathway in cancer cells, fulfilling their energy requirements, supporting biosynthesis, maintaining redox balance, and enabling survival hostile environments. Alpha-enolase (ENO1) has been identified as key promoter of tumor progression through its involvement glycolysis. This study aims to elucidate the relationship between ENO1, glycolysis, gemcitabine sensitivity pancreatic (PC). The expression levels ENO1 PC were analyzed using GEPIA2 database, Kaplan-Meier plots, immunohistochemistry (IHC). To assess impact on sensitivity, we manipulated cell lines overexpression silencing techniques. Subsequent analyses included flow cytometry assays, glucose uptake lactate production measurements, cytotoxicity assays. underlying mechanisms by which modulates explored Western blotting (WB). was found be significantly overexpressed tissues, elevated associated with poorer prognosis patients. Overexpression reduced cells gemcitabine, enhancing proliferation, migration, invasion altering cycle inhibiting apoptosis. Conversely, decreased glycolysis heightened gemcitabine. Furthermore, inhibition—achieved knockdown, deprivation, or treatment 2-Deoxy-D-glucose (2-DG)—further enhanced susceptibility Mechanistically, regulate resistance-related genes, particularly ribonucleotide reductase catalytic subunit M1 (RRM1), via MYC glycolytic pathway, thereby contributing resistance. demonstrates that plays crucial role closely linked resistance regulation pathway.

Язык: Английский

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ENO2, a Glycolytic Enzyme, Contributes to Prostate Cancer Metastasis: A Systematic Review of Literature

Cancers, Год журнала: 2024, Номер 16(14), С. 2503 - 2503

Опубликована: Июль 10, 2024

Prostate cancer (PCa) is the second leading cause of male deaths in UK and fifth worldwide. The presence distant PCa metastasis can reduce 5-year survival rate from 100% to approximately 30%. Enolase 2 (ENO2), a crucial glycolytic enzyme metabolism, associated with multiple cancers also used as marker for neuroendocrine tumours. However, its role remains unclear. In this study, we systematically reviewed current literature determine association between ENO2 metastatic PCa. Medline, Web Science, PubMed were searched eligible studies. search yielded five studies assessing expression patients or cell lines. three human suggested that correlated late-stage, aggressive PCa, including castrate-resistant (CRPC), CRPC, (NEPC). This was further supported by two vitro indicating be regulated tumour microenvironment, such androgen deprived conditions bone-forming osteoblasts. Therefore, may functionally contribute metastasis, possibly due unique metabolic features which are glycolysis dependent only at advanced stage.

Язык: Английский

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HOXC6‐mediated transcriptional activation of ENO2 promotes oral squamous cell carcinoma progression through the Warburg effect

Journal of Biochemical and Molecular Toxicology, Год журнала: 2024, Номер 38(7)

Опубликована: Июнь 23, 2024

Abstract Oral squamous cell carcinoma (OSCC) requires an in‐depth exploration of its molecular mechanisms. The Warburg effect, along with the oncogenes enolase 2 (ENO2) and homeobox C6 (HOXC6), plays a central role in cancer. However, specific interaction between ENO2 HOXC6 driving effect OSCC progression remains poorly understood. Through differential gene expression analysis head neck carcinomas using Gene Expression Profiling Interactive Analysis, we identified upregulated OSCC. Silencing cells revealed involvement migration, invasion, aerobic glycolysis cells. Further ENO2's regulatory network as potential transcriptional regulator. Subsequently, was silenced cells, expressions were assessed to validate relationship ENO2. Chromatin Immunoprecipitation luciferase assays utilized investigate direct activation by HOXC6. A rescue assay co‐overexpressing silencing affirmed HOXC6's ENO2‐associated glycolysis. High validated through quantitative real‐time polymerase chain reaction, Western blot, immunohistochemistry analyses, which correlated poor patient survival. Functional demonstrated that inhibited attenuated aggressiveness In vivo studies confirmed oncogenic growth. Notably, exhibited positive correlation clinical samples. Mechanistically, activator ENO2, orchestrating This study reveals intricate link HOXC6‐mediated OSCC, offering therapeutic target for treating patients.

Язык: Английский

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ENO2 in Progression and Treatment of Colon Adenocarcinoma Based on Non-Apoptotic Cell Death

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Июль 19, 2024

Colon adenocarcinoma (COAD) is one of the most common types cancer. The interconnection between non-apoptotic cell death and COAD has not been adequately addressed. In our study, an integrative computational analysis was performed to explore death-related biomarkers in COAD. ENO2 determined as a potent biomarker for prognosis, drug response, immunity, immunotherapy prediction. We used EdU RT-qPCR assays test hypothesis investigate how gene may influence or regulate cancer-related processes. expected be potential target

Язык: Английский

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ENO2 in progression and treatment of colon adenocarcinoma: integrative bioinformatics analysis on non-apoptotic cell death

Discover Oncology, Год журнала: 2024, Номер 15(1)

Опубликована: Сен. 27, 2024

Язык: Английский

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