ArticleCancer science2021
Specific activation of glycolytic enzyme enolase 2 in BRAF V600E-mutated colorectal cancer.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- A comprehensive overview of the molecular features and therapeutic targets in BRAFClinical and translational medicine · 2024Pooled it
- ENO2 sustains cancer stemness and metastatic competence through a phosphoenolpyruvate-dependent metabolic axis in triple-negative breast cancer.Cell death & disease · 2026Article
- Inhibition of FOS-Like Antigen 1 Reduces Chemoresistance to Temozolomide Through Stemness Reprogramming via IL-6/STAT3MedComm · 2026Article
- Mannose enhances anti-tumor effect of PLX4032 in anaplastic thyroid cancer.Endocrine-related cancer · 2025Article
- FOSL1 transcriptionally dictates the Warburg effect and enhances chemoresistance in triple-negative breast cancer.Journal of translational medicine · 2025Article
- Understanding the Molecular Mechanisms of Incomptine A in Treating Non-Hodgkin Lymphoma Associated with U-937 Cells: Bioinformatics Approaches, Part I.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Prediction of overall survival in stage II and III colon cancer through machine learning of rapidly-acquired proteomics.Cell discovery · 2024Article
- ENO2, a Glycolytic Enzyme, Contributes to Prostate Cancer Metastasis: A Systematic Review of Literature.Cancers · 2024Review
- Investigation of ENO2 as a promising novel marker for the progression of colorectal cancer with microsatellite instability-high.BMC cancer · 2024Article
- BeyondMolecular therapy oncolytics · 2023Review
- Toward Systems-Level Metabolic Analysis in Endocrine Disorders and Cancer.Endocrinology and metabolism (Seoul, Korea) · 2023Review
- ENO2-derived phosphoenolpyruvate functions as an endogenous inhibitor of HDAC1 and confers resistance to antiangiogenic therapy.Nature metabolism · 2023Article
- Targeting ARF1-IQGAP1 interaction to suppress colorectal cancer metastasis and vemurafenib resistance.Journal of advanced research · 2023Article
- Immune checkpoint blockade therapy for BRAF mutant metastatic colorectal cancer: the efficacy, new strategies, and potential biomarkers.Discover oncology · 2023Review
- Long noncoding RNA 01534 maintains cancer stemness by downregulating endoplasmic reticulum stress response in colorectal cancer.Annals of gastroenterological surgery · 2023Article
- ALDOC- and ENO2- driven glucose metabolism sustains 3D tumor spheroids growth regardless of nutrient environmental conditions: a multi-omics analysis.Journal of experimental & clinical cancer research : CR · 2023Article
- Aerobic glycolysis in colon cancer is repressed by naringin via theJournal of Zhejiang University. Science. B · 2023Article
- Understanding the Contribution of Lactate Metabolism in Cancer Progress: A Perspective from Isomers.Cancers · 2022Review
- Article
- Identification of ENO1 as a prognostic biomarker and molecular target among ENOs in bladder cancer.Journal of translational medicine · 2022Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
The BRAF V600E mutation occurs in approximately 10% of patients with metastatic colorectal cancer (CRC) and constitutes a distinct subtype of the disease with extremely poor prognosis. To address this refractory disease, we investigated the unique metabolic gene profile of BRAF V600E-mutated tumors via in silico analysis using a large-scale clinical database. We found that BRAF V600E-mutated tumors exhibited a specific metabolic gene expression signature, including some genes that are associated with poor prognosis in CRC. We discovered that BRAF V600E-mutated tumors expressed high levels of glycolytic enzyme enolase 2 (ENO2), which is mainly expressed in neuronal tissues under physiological conditions. In vitro experiments using CRC cells demonstrated that BRAF V600E-mutated cells exhibited enhanced dependency on ENO2 compared to BRAF wild-type cancer cells and that knockdown of ENO2 led to the inhibition of proliferation and migration of BRAF V600E-mutated cancer cells. Moreover, inhibition of ENO2 resulted in enhanced sensitivity to vemurafenib, a selective inhibitor of BRAF V600E. We identified AP-1 transcription factor subunit (FOSL1) as being involved in the transcription of ENO2 in CRC cells. In addition, both MAPK and PI3K/Akt signaling were suppressed upon inhibition of ENO2, implying an additional oncogenic role of ENO2. These results suggest the crucial role of ENO2 in the progression of BRAF V600E-mutated CRC and indicate the therapeutic implications of targeting this gene.
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