ArticleOncoTargets and therapy2020
The Pseudogene DUXAP8 Promotes Colorectal Cancer Cell Proliferation, Invasion, and Migration by Inducing Epithelial-Mesenchymal Transition Through Interacting with EZH2 and H3K27me3.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- ORANGE: a machine learning approach for modeling tissue-specific aging from transcriptomic data.Briefings in bioinformatics · 2026Article
- DNA, RNA, and histone methylation regulation enzymes and their crosstalk in colorectal carcinogenesis and progression: a review of molecular mechanisms, clinical implications, and future perspectives.Cellular & molecular biology letters · 2025Review
- Histone Modification of Colorectal Cancer by Natural Products.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Non-coding RNAs as emerging regulators and biomarkers in colorectal cancer.Molecular and cellular biochemistry · 2022Review
- LncRNA MSTO2P promotes colorectal cancer progression through epigenetically silencing CDKN1A mediated by EZH2.World journal of surgical oncology · 2022Article
- The long and short non-coding RNAs modulating EZH2 signaling in cancer.Journal of hematology & oncology · 2022Review
- Functions of lncRNA DUXAP8 in non-small cell lung cancer.Molecular biology reports · 2022Review
- Long non-coding RNAs as the critical regulators of epithelial mesenchymal transition in colorectal tumor cells: an overview.Cancer cell international · 2022Review
- LncRNAFrontiers in genetics · 2022Article
- Pseudogenes and Liquid Phase Separation in Epigenetic Expression.Frontiers in oncology · 2022Review
- Whole genome sequencing of Malaysian colorectal cancer patients reveals specific druggable somatic mutations.Frontiers in molecular biosciences · 2022Article
- CMAHP promotes metastasis by reducing ubiquitination of Snail and inducing angiogenesis via GM-CSF overexpression in gastric cancer.Oncogene · 2022Article
- Development and validation of ferroptosis-related lncRNAs prognosis signatures in kidney renal clear cell carcinoma.Cancer cell international · 2021Article
- A Comprehensive Analysis of SE-lncRNA/mRNA Differential Expression Profiles During Chondrogenic Differentiation of Human Bone Marrow Mesenchymal Stem Cells.Frontiers in cell and developmental biology · 2021Article
- Long Non-coding RNA Double Homeobox A Pseudogene 8: A Novel Oncogenic Propellant in Human Cancer.Frontiers in cell and developmental biology · 2021Review
- Analysis of Long Noncoding RNAs in Aila-Induced Non-Small Cell Lung Cancer Inhibition.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer (CRC) is the third leading cause of cancer death worldwide. The long noncoding RNA (lncRNA) DUXAP8 has been reported to play an important role in CRC. This study investigated the mechanism by which this lncRNA regulates CRC progression.
methodsThe levels of lncRNA DUXAP8 in CRC tissues and cell lines were detected by qRT-PCR. We then knocked down or forced overexpression of DUXAP8, and the resultant effect on cell proliferation was determined by the Edu assay and a cell cycle analysis, and the effect on cell apoptosis was determined by flow cytometry. The cell invasion/migration ability and the epithelial-to-mesenchymal transition (EMT) markers were determined by Transwell/wound healing assays and Western blotting. CHIP and RNA pull-down assays were performed to determine the binding of Zeste gene enhancer 2 (EZH2) and trimethylated histone H3 to Lys27 (H3K27me3) in the E-cadherin promoter regions, or to DUXAP8.
resultsThe levels of lncRNA DUXAP8 were significantly increased in CRC tissues and CRC cell lines. Knockdown of lncRNA DUXAP8 inhibited cell proliferation and the EMT process, and increased cell apoptosis, and overexpression of lncRNA DUXAP8 had an opposite effect. Both ChIP and RNA pull-down assays showed that the E-cadherin promoter region was bound by H3K27me3 and EZH2, which restrained E-cadherin expression. However, that binding was suppressed and E-cadherin expression was markedly induced by lncRNA DUXAP8 knockdown. Furthermore, lncRNA DUXAP8 could interact with EZH2 and H3K27me3.
conclusionOur data indicated that lncRNA DUXAP8 could induce the progression of CRC by negatively regulating E-cadherin via interaction with EZH2 and H3K27me3. These findings suggest lncRNA DUXAP8 as target for treating CRC.
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