ArticleBMC cancer2015
Epigenetic regulation of CDH1 exon 8 alternative splicing in gastric cancer.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- The role of alternative splicing in gastric cancer.Biology direct · 2026Review
- Splicing regulatory dynamics for precision analysis and treatment of heterogeneous leukemias.Science translational medicine · 2025Article
- Exploring the mechanism of ellagic acid against gastric cancer based on bioinformatics analysis and network pharmacology.Journal of cellular and molecular medicine · 2023Article
- Alternative Splicing, Epigenetic Modifications and Cancer: A Dangerous Triangle, or a Hopeful One?Cancers · 2022Review
- Article
- H3K36 trimethylation-mediated biological functions in cancer.Clinical epigenetics · 2021Review
- Noncoding RNAs regulate alternative splicing in Cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- Integrated Assessment of Viral Transcription, Antigen Presentation, and CD8Journal of virology · 2020Article
- Involvement of SLC39A6 in gastric adenocarcinoma and correlation of the SLC39A6 polymorphism rs1050631 with clinical outcomes after resection.BMC cancer · 2019Article
- Regulation of alternative splicing by p300-mediated acetylation of splicing factors.RNA (New York, N.Y.) · 2019Article
- The E-Cadherin Cleavage Associated to Pathogenic Bacteria Infections Can Favor Bacterial Invasion and Transmigration, Dysregulation of the Immune Response and Cancer Induction in Humans.Frontiers in microbiology · 2019Review
- Transcriptome-wide analysis of alternative mRNA splicing signature in the diagnosis and prognosis of stomach adenocarcinoma.Oncology reports · 2018Article
- Exploiting differential RNA splicing patterns: a potential new group of therapeutic targets in cancer.Expert opinion on therapeutic targets · 2018Review
- Influence of transcriptional variants on metastasis.RNA biology · 2018Review
- Article
- SETD2: an epigenetic modifier with tumor suppressor functionality.Oncotarget · 2016Review
- Promoter methylation and expression of CDH1 and susceptibility and prognosis of eyelid squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- The association, clinicopathological significance, and diagnostic value ofOncoTargets and therapy · 2016Article
- Low H3K9me3 Expression Is Associated With Poor Prognosis in Patients With Distal Common Bile Duct Cancer.In vivo (Athens, Greece)Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe tumor suppressor gene CDH1 is critical for intercellular adhesion. In our previous work, we reported a nonfunctional CDH1 transcript that lacks the final 83 base pairs of exon 8 (1054del83). In this work, we probed the role of histone epigenetic modifications as well as DNA methylation in selection of this isoform.
methodsRT-qPCR was used to detect CDH1 RNA expression. Methylation of CDH1 was analyzed by bisulphite sequencing PCR. ChIP assay was performed to show histones level. Cell lines were treated with DNA methyltransferase inhibitor AZA, HDAC inhibitor TSA, or siRNA oligonucleotides to test regulation of CDH1 splicing.
resultsGreater CDH1 1054del83 transcripts were observed in gastric cancer (GC) cell lines than human gastric mucosal epithelial cell line GES-1. All the cell lines showed significant methylation pattern at the CpG sites of CDH1 exon 8. AZA treatment did not influence selection of 1054del83 transcripts. A significant decrease in acetylation for histones H3 and H4K16Ac in an internal region of the CDH1 gene surrounding the alternative exon 8 were detected in GC cell lines. Treatment with TSA preferentially expressed the correctly spliced transcript and not the exon 8 skipped aberrant transcripts, showing that histone acetylation was involved in the splicing regulation. SiRNA-mediated knockdown of SETD2 (The specific methyltransferase of H3K36) decreased exclusion of exon 8, suggesting that the presence of this mark correlates with increased skipping of the final 83 base pairs of CDH1 exon 8. However, CDH1 splicing was not affected by SRSF2 knockdown.
conclusionsH3K36me3 correlates with increased skipping of the final 83 base pairs of CDH1 exon 8. Histone acetylation was involved in the splicing regulation as well.
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