ArticleClinical epigenetics2022
LINC00114 stimulates growth and glycolysis of esophageal cancer cells by recruiting EZH2 to enhance H3K27me3 of DLC1.
Article in Clinical epigenetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 18 citations in OpenAlex.
- Data-driven discovery of gene expression markers distinguishing pediatric acute lymphoblastic leukemia subtypes.Molecular oncology · 2025Article
- Review
- LINC00114 promotes colorectal cancer metastasis by targeting HNRNPA1 to regulate glutamine metabolism reprogramming and angiogenesis.Acta biochimica et biophysica Sinica · 2025Article
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- The role of LINC00114 in atopic dermatitis: modulating inflammation and epidermal barrier dysfunction.Archives of dermatological research · 2025Article
- Long non-coding RNAs in humans: Classification, genomic organization and function.Non-coding RNA research · 2025Review
- Absence of Scaffold Protein Tks4 Disrupts Several Signaling Pathways in Colon Cancer Cells.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveLINC00114 could promote the development of colorectal cancer, but its mechanism has been rarely discussed in esophageal cancer (EC). Herein, we explored the molecular mechanism of LINC00114 via mediating enhancer of zeste homolog 2/deleted in liver cancer 1 (EZH2/DLC1) axis in EC.
methodsLINC00114, EZH2 and DLC1 expression in EC tissues and cells were tested. LINC00114, EZH2 and DLC1 expression were altered in EC cells through transfection with different constructs, and cell proliferation, migration, invasion, apoptosis and glycolysis were subsequently observed. The interaction between LINC00114 and EZH2 and that between EZH2 and DLC1 were explored. Tumor formation was also conducted to confirm the in vitro results.
resultsThe expression levels of LINC00114 and EZH2 were elevated while those of DLC1 were reduced in EC. Inhibiting LINC00114 or reducing EZH2 blocked cell proliferation, migration, invasion and glycolysis and induce cell apoptosis in EC. LINC00114 promoted H3K27 trimethylation of DLC1 by recruiting EZH2. Knockdown of DLC1 stimulated cell growth and glycolysis in EC and even mitigated the role of LINC00114 inhibition in EC. In vivo experiment further confirmed the anti-tumor effect of LINC00114 inhibition in EC.
conclusionThe data indicate that LINC00114 promotes the development of EC by recruiting EZH2 to enhance H3K27me3 of DLC1.
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Registered trials
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