ArticleBMC cancer2012
Promoter hypermethylation-induced transcriptional down-regulation of the gene MYCT1 in laryngeal squamous cell carcinoma.
Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- UVB Upregulates Inflammatory Cytokines in Rosacea Cell Model by Promoting the Expression of TRPVs and TLR2.ImmunoTargets and therapy · 2026Article
- MYCT-1 Gene Expression in Patients with Gastric Cancer: an Ex Vivo Study.Applied biochemistry and biotechnology · 2024Article
- Differentially expressed genes related to lymph node metastasis in advanced laryngeal squamous cell cancers.Oncology letters · 2022Article
- The role of DNA methylation in syndromic and non-syndromic congenital heart disease.Clinical epigenetics · 2021Review
- The Evi5 oncogene promotes laryngeal cancer cells proliferation by stabilizing c-Myc protein.Cancer cell international · 2020Article
- Aberrant methylation and downregulation of ZNF667-AS1 and ZNF667 promote the malignant progression of laryngeal squamous cell carcinoma.Journal of biomedical science · 2019Article
- [Long chain non-coding RNA MALAT-1 gene knockdown inhibits growth and migration and promotes apoptosis of human laryngeal squamous cell carcinoma Hep-2 cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- Overexpression of MYCT1 Inhibits Proliferation and Induces Apoptosis in Human Acute Myeloid Leukemia HL-60 and KG-1a CellsFrontiers in pharmacology · 2018Article
- YY1 directly suppresses MYCT1 leading to laryngeal tumorigenesis and progress.Cancer medicine · 2017Article
- RNA-seq transcriptome analysis of formalin fixed, paraffin-embedded canine meningioma.PloS one · 2017Article
- Article
- An Epigenetic Mechanism of High Gdnf Transcription in Glioma Cells Revealed by Specific Sequence Methylation.Molecular neurobiology · 2016Article
- SSTR2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males.Diagnostic pathology · 2016Article
- CITED2 mutation and methylation in children with congenital heart disease.Journal of biomedical science · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMYCT1, previously named MTLC, is a novel candidate tumor suppressor gene. MYCT1 was cloned from laryngeal squamous cell cancer (LSCC) and has been found to be down-regulated in LSCC; however, the regulatory details have not been fully elucidated.
methodsHere, we sought to investigate the methylation status of the CpG islands of MYCT1 and mRNA levels by bisulfite-specific PCR (BSP) based on sequencing restriction enzyme digestion, reverse transcription and real-time quantitative polymerase chain reaction (RQ-PCR). The function of specific sites in the proximal promoter of MYCT1 in LSCC was measured by transient transfection, luciferase assays, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation assay (ChIP).
resultsThe results suggested hypermethylation of 12 CpG sites of the promoter in both laryngeal cancer tissues and the laryngeal cancer line Hep-2 cell. The hypermethylation of the site CGCG (-695 to -692), which has been identified as the c-Myc binding site, was identified in laryngeal cancer tissues (59/73) compared to paired mucosa (13/73); in addition, statistical analysis revealed that the methylation status of this site significantly correlated with cancer cell differentiation(p < 0.01). The mRNA level of MYCT1 increased in Hep-2 cells treated with 5-aza-C (p < 0.01). The luciferase activity from mutant transfectants pGL3-MYCT1m (-852/+12, mut-695-C > A, mut-693-C > G) was significantly reduced compared with the wild type pGL3-MYCT1 (-852/+12), while the luciferase activity from wild transfectants pGL3-MYCT1 (-852/+12) rose after 5-aza treatment in Hep-2 cells. Finally, EMSA and ChIP confirmed that the methylation of the CGCG (-695 to -692) site prevented c-Myc from binding of the site and demethylation treatment of the 5' flanking region of MYCT1 by 5-aza induced the increased occupation of the core promoter by c-Myc (p < 0.01).
conclusionIn summary, this study concluded that hypermethylation contributed to the transcriptional down-regulation of MYCT1 and could inhibit cancer cell differentiation in LSCC. DNA methylation of the CGCG site (-695 to -692) of MYCT1 altered the promoter activity by interfering with its binding to c-Myc in LSCC. Epigenetic therapy of reactivating MYCT1 by 5-aza should be further evaluated in clinical trails of LSCC.
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