Ask about this productRelated genes to: ENO2 Blocking Peptide
- Gene:
- ENO2 NIH gene
- Name:
- enolase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-04-28
Related products to: ENO2 Blocking Peptide
Related articles to: ENO2 Blocking Peptide
- Neuroendocrine prostate cancer (NEPC) is an aggressive treatment-associated lineage state emerging with potent androgen receptor (AR) pathway inhibition. Although treatment-emergent NEPC is increasingly recognized, the transcriptional consequences of sustained AR suppression remain incompletely defined. It remains unclear to what extent AR-targeted therapies reshape cellular identity and engage neuroendocrine-associated transcriptional programs without full lineage-defining differentiation. - Source: PubMed
Publication date: 2026/07/24
Watanabe RyutaChosei MamiArai HarunaMiura NoriyoshiKikugawa TadahikoSaika Takashi - CSF proteomics has emerged as a valuable strategy for identifying diagnostic and prognostic biomarkers in amyotrophic lateral sclerosis (ALS). However, the limited availability and volumes of CSF samples restrict the broader clinical application of CSF-based biomarker panels. To address this challenge, we investigated whether the novel nucleic acid-linked immuno-sandwich assay (NULISA) multiplex platform-capable of quantifying multiple neural, glial, and inflammatory markers from minimal biofluid volumes-could validate previously proposed biomarkers and identify additional candidates relevant to ALS. - Source: PubMed
Publication date: 2026/07/14
Baskar KarthikSteffke ChristinaBernsen SarahElmas ZeynepHesebeck-Brinckmann JasperSchuster JoachimMeyer ThomasWeydt PatrickWeishaupt JochenBrenner DavidCatanese Alberto - Clear cell renal cell carcinoma (ccRCC) exhibits glycolytic addiction due to VHL mutation, making it vulnerable to metabolic intervention. While conventional inhibitors targeting core housekeeping glycolytic enzymes show robust antitumor efficacy, their clinical use is limited by on-target systemic toxicity. Here, we identify enolase 2 (ENO2) as an isoform-specific glycolytic vulnerability specific to VHL-deficient ccRCC. Although ENO2 is physiologically redundant (compensated by ENO1) in normal glycolysis, it becomes essential for sustaining ccRCC malignancy via VHL loss-HIF2α-driven glycolytic flux. Targeting ENO2 specifically suppressed glycolysis in VHL-deficient ccRCC cells, reducing their malignancy and enhancing their response to axitinib, doxorubicin, and gemcitabine. Importantly, pharmacological ENO2 blockade displayed superior tumor selectivity compared to traditional glycolysis inhibitors, effectively eliminating VHL-deficient ccRCC cells while sparing VHL-intact normal and malignant cells, despite causing slightly weaker glycolytic suppression. Mechanistic investigations revealed that ENO2 ablation inactivated up to ~78% of VHL loss-induced oncogenic effectors, including a pleiotropic oncoprotein MDK, through dual modulation of lactate metabolism and interferon signaling. Collectively, this work reveals ENO2 as a genotype-specific metabolic dependency in ccRCC, thereby enabling precision glycolytic therapy. Our work also suggests that targeting physiologically redundant metabolic isoenzymes may offer a precision medicine strategy for cancers with defined genetic alterations. - Source: PubMed
Publication date: 2026/07/14
Yao JiannanFan XiaonaXin HuixianWan FuhuiDong XichenSun QianqianHuang XuyingLiu HeshuChen XiangyuJia YanjunQian HailiWen TaoLiu Jian - Blood-based biomarkers are increasingly recognized as promising tools for the diagnosis and monitoring of neurodegenerative diseases, offering a minimally invasive alternative to cerebrospinal fluid (CSF) testing. We evaluated the analytical performance and clinical utility of the Olink Target 48 Neurodegeneration panel, a novel multiplex proteomic platform based on the proximity extension assay (PEA) technology, in a large, clinically diverse dementia cohort. - Source: PubMed
Publication date: 2026/07/11
Bentivenga Giuseppe MarioMammana AngelaBaiardi SimoneVittoriosi EricaMastrangelo AndreaRuggeri EdoardoVargiu Claudia MarinaPolischi BarbaraStanzani-Maserati MichelangeloRizzo GiovanniPantieri RobertaRaggi AlbertoCapellari SabinaParchi Piero - Enolase 2 (ENO2) is a neuron-specific glycolytic enzyme whose expression is elevated in aggressive breast cancers, yet its enzymatic and biological contributions to triple-negative breast cancer (TNBC) progression remain incompletely defined. Here, we demonstrate that ENO2 sustains cancer stem cell (CSC) properties and metastatic competence through a phosphoenolpyruvate (PEP)-dependent metabolic axis. Elevated ENO2 expression correlated with advanced tumor grade and poor clinical outcomes in TNBC cohorts, underscoring its clinical relevance. Genetic depletion of ENO2 impaired aerobic glycolysis and oxidative phosphorylation, reduced migration, invasion, and CSC frequency, and suppressed tumor growth and pulmonary metastasis in orthotopic models. Mechanistically, exogenous PEP or pyruvate restored CSC-associated traits and invasiveness in ENO2-deficient cells, supporting the functional involvement of ENO2-derived metabolites in CSC maintenance. Reconstitution with wild-type ENO2, but not a catalytically impaired mutant, restored CSC properties, invasiveness, and metastatic colonization, establishing that ENO2 catalytic activity is required for these malignant traits. Further analysis revealed that PKM2 perturbation preferentially attenuated PEP-mediated rescue while largely sparing pyruvate-mediated rescue, supporting a functional PEP-PKM2-pyruvate axis in CSC regulation. Consistently, PKM2 depletion partially blunted ENO2-mediated rescue; however, residual rescue despite PKM2 perturbation suggested additional PKM2-independent PEP-responsive mechanisms. Importantly, pharmacological inhibition of enolase with POMHEX phenocopied genetic ENO2 loss and suppressed CSC maintenance in vitro and tumor growth in vivo. Taken together, these findings identify the ENO2-driven PEP-dependent metabolic axis as a mechanistic link between metabolic reprogramming, cancer stemness, and metastasis, revealing a therapeutically actionable metabolic vulnerability in TNBC. - Source: PubMed
Publication date: 2026/07/11
Wang Cing-HongMai Ru-TsunKhoo Ke JiaHung Chi-FengYang Cheng-KuangWu Meng-JuChao Chi-Hong