ArticleOncotarget2015
Enolase-1 is a therapeutic target in endometrial carcinoma.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 63 citations in OpenAlex.
- Bioinformatic Approach to Identify Positive PrognosticInternational journal of molecular sciences · 2025Article
- Clinical implications of epithelial-to-mesenchymal transition in cancers which potentially spread to peritoneum.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Genome-scale modeling identifies dynamic metabolic vulnerabilities during the epithelial to mesenchymal transition.Communications biology · 2024Article
- Identification of ENO-1 positive extracellular vesicles as a circulating biomarker for monitoring of Ewing sarcoma.Cancer science · 2024Article
- SMYD3 promotes endometrial cancer through epigenetic regulation of LIG4/XRCC4/XLF complex in non-homologous end joining repair.Oncogenesis · 2024Article
- KAT2A changes the function of endometrial stromal cells via regulating the succinylation of ENO1.Open life sciences · 2024Article
- Identification and subsequent validation of transcriptomic signature associated with metabolic status in endometrial cancer.Scientific reports · 2023Article
- Article
- Exploring breast cancer exosomes for novel biomarkers of potential diagnostic and prognostic importance.3 Biotech · 2023Article
- Essential role of aerobic glycolysis in epithelial-to-mesenchymal transition during carcinogenesis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- A Novel Enolase-1 Antibody Targets Multiple Interacting Players in the Tumor Microenvironment of Advanced Prostate Cancer.Molecular cancer therapeutics · 2022Article
- TRPC5OS induces tumorigenesis by increasing ENO1-mediated glucose uptake in breast cancer.Translational oncology · 2022Article
- Proteomic Analysis of Endometrial Cancer Tissues from Patients with Type 2 Diabetes Mellitus.Life (Basel, Switzerland) · 2022Article
- Endometrial Cancer Stem Cells: Where Do We Stand and Where Should We Go?International journal of molecular sciences · 2022Review
- ENO1 and Cancer.Molecular therapy oncolytics · 2022Review
- Reprogramming Carbohydrate Metabolism in Cancer and Its Role in Regulating the Tumor Microenvironment.Sub-cellular biochemistry · 2022Article
- Homocitrullination of lysine residues mediated by myeloid-derived suppressor cells in the tumor environment is a target for cancer immunotherapy.Journal for immunotherapy of cancer · 2021Article
- Article
- α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1.Frontiers in cell and developmental biology · 2021Article
- Nuclear Enolase-1/ MBP-1 expression and its association with the Wnt signaling in epithelial ovarian cancer.Translational oncology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ENO1 plays a paradoxical role in driving the pathogenesis of tumors. However, the clinical significance of ENO1 expression remains unclear and its function and modulatory mechanisms have never been reported in endometrial carcinoma (EC). In this study, ENO1 silencing significantly reduced cell glycolysis, proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo by modulating p85 suppression. This in turn mediated inactivation of PI3K/AKT signaling and its downstream signals including glycolysis, cell cycle progression, and epithelial-mesenchymal transition (EMT)-associated genes. These effects on glycolysis and cell growth were not observed after ENO1 suppression in normal human endometrial epithelial cells (HEEC). Knocking down ENO1 could significantly enhance the sensitivity of EC cells to cisplatin (DDP) and markedly inhibited the growth of EC xenografts in vivo. In clinical samples, EC tissues exhibited higher expression levels of ENO1 mRNA and protein compared with normal endometrium tissues. Patients with higher ENO1 expression had a markedly shorter overall survival than patients with low ENO1 expression. We conclude that ENO1 favors carcinogenesis, representing a potential target for gene-based therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.