ArticleTechnology in cancer research & treatment2018
Silencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cancer Cells.
Article in Technology in cancer research & treatment, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Glycolysis‑driven immunosuppression in gastric cancer: Metabolic crosstalk between tumor cells and the immune microenvironment (Review).International journal of oncology · 2026Review
- ENO1 as a Central Regulator Linking Metabolic Reprogramming to Tumor Plasticity.International journal of molecular sciences · 2026Review
- Review
- SENP1 drives glycolysis and cisplatin resistance in gastric cancer via desumoylating ENO1.Journal of experimental & clinical cancer research : CR · 2025Article
- RNA-binding proteinJournal of gastrointestinal oncology · 2023Article
- TRPC5OS induces tumorigenesis by increasing ENO1-mediated glucose uptake in breast cancer.Translational oncology · 2022Article
- Effects of urolithin A on osteoclast differentiation induced by receptor activator of nuclear factor-κB ligand via bone morphogenic protein 2.Bioengineered · 2022Article
- Article
- Parathyroid hormone type 1 receptor regulates osteosarcoma K7M2 Cell growth by interacting with angiotensinogen.Journal of cellular and molecular medicine · 2021Article
- Introducing physical exercise as a potential strategy in liver cancer prevention and development.Gastroenterology and hepatology from bed to bench · 2021Article
- Enolase 1 regulates stem cell-like properties in gastric cancer cells by stimulating glycolysis.Cell death & disease · 2020Article
- Prognostic Value of Enolase Gene Family in Colon Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Metabolic Pathways Enhancement Confers Poor Prognosis in p53 Exon Mutant Hepatocellular Carcinoma.Cancer informatics · 2020Article
- Penalized logistic regression based on L1/2 penalty for high-dimensional DNA methylation data.Technology and health care : official journal of the European Society for Engineering and Medicine · 2020Article
- The circ-AMOTL1/ENO1 Axis Implicated in the Tumorigenesis of OLP-Associated Oral Squamous Cell Carcinoma.Cancer management and research · 2020Article
- Alpha-Enolase: Emerging Tumor-Associated Antigen, Cancer Biomarker, and Oncotherapeutic Target.Frontiers in genetics · 2020Review
- Up-regulated ENO1 promotes the bladder cancer cell growth and proliferation via regulating β-catenin.Bioscience reports · 2019Article
- Hyperglycemia promotes Snail-induced epithelial-mesenchymal transition of gastric cancer via activating ENO1 expression.Cancer cell international · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
α-Enolase is a significant subunit of enolase and acts as a glycolytic enzyme responsible for catalyzing the conversion of 2-phosphoglycerate to phosphoenolpyruvate in the anaerobic glycolysis pathway. The research about their role is known little in tumor invasion and metastasis. This research analyzed the effect of α-enolase in proliferation and progression of human gastric cancer. The constructed PLKO.1-ENO1 shRNA vector was transfected into 293 T cells and used to infect gastric cancer cells, MKN45, by using lentivirus method. Negative controls were generated by infection with viruses containing empty vector PLKO.1-scramble-shRNA by the same protocol and using wild-type MKN45 cells as blank control. The silencing effect was confirmed by reverse transcription polymerase chain reaction and Western blotting at messenger RNA and protein levels, respectively. Cell proliferation and chemosensitivity were tested by methyl-thiazolyl-tetrazolium assay. Cell apoptosis was tested by flow cytometry. The cell line α-enolase short hairpin RNA stabling silence α-enolase was successfully constructed. In the α-enolase short hairpin RNA cell lines, messenger RNA and protein expression of α-enolase were significantly lower than those in negative control and blank control groups. The proliferation and clone formation ability were significantly inhibited, cell apoptosis was increased significantly, and the inhibition rate of chemotherapy drugs was increased ( P < .05). Our data provide strong evidence that α-enolase short hairpin RNA interference vector can effectively suppress the proliferation and increase chemosensitivity of MKN45 cells, which may provide a novel gene therapy for gastric cancer.
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Registered trials
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