ArticleThe American journal of pathology2010
Epigenetic silencing of a proapoptotic cell adhesion molecule, the immunoglobulin superfamily member IGSF4, by promoter CpG methylation protects Hodgkin lymphoma cells from apoptosis.
Article in The American journal of pathology, 2010. 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, 23 citations in OpenAlex.
- Article
- Clinical significance of soluble CADM1 as a novel marker for adult T-cell leukemia/lymphoma.Haematologica · 2021Article
- Low Expression and Promoter Hypermethylation of the Tumour Suppressor SLIT2, are Associated with Adverse Patient Outcomes in Diffuse Large B Cell Lymphoma.Pathology oncology research : POR · 2019Article
- Change of Immunoglobulin Superfamily Member 4 Gene Expression in the Digestive System after Swimming Exercise in BALB/c Mice.Iranian journal of public health · 2018Article
- Epstein-Barr Virus-Induced Epigenetic Pathogenesis of Viral-Associated Lymphoepithelioma-Like Carcinomas and Natural Killer/T-Cell Lymphomas.Pathogens (Basel, Switzerland) · 2018Review
- Chidamide and decitabine can synergistically induce apoptosis of Hodgkin lymphoma cells by up-regulating the expression of PU.1 and KLF4.Oncotarget · 2017Article
- Mutual regulation of microRNAs and DNA methylation in human cancers.Epigenetics · 2017Review
- Epigenetic inactivation of the CpG demethylase TET1 as a DNA methylation feedback loop in human cancers.Scientific reports · 2016Article
- Hypermethylation of the 16q23.1 tumor suppressor gene ADAMTS18 in clear cell renal cell carcinoma.International journal of molecular sciences · 2015Article
- Genetic methylation and lymphoid malignancies: biomarkers of tumor progression and targeted therapy.Biomarker research · 2013Article
- Epigenetic silencing of the 3p22 tumor suppressor DLEC1 by promoter CpG methylation in non-Hodgkin and Hodgkin lymphomas.Journal of translational medicine · 2012Article
- The collagen prolyl hydroxylases are novel transcriptionally silenced genes in lymphoma.British journal of cancer · 2012Article
- Hypomethylation and Over-Expression of the Beta Isoform of BLIMP1 is Induced by Epstein-Barr Virus Infection of B Cells; Potential Implications for the Pathogenesis of EBV-Associated Lymphomas.Pathogens (Basel, Switzerland) · 2012Article
- Hypermethylation of IGSF4 gene for noninvasive prenatal diagnosis of thalassemia.Medical science monitor : international medical journal of experimental and clinical research · 2012Article
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Authors and funding
18 authors at 6 institutions in 5 countries.
Funding
Abstract
The malignant Hodgkin/Reed-Sternberg (HRS) cells of Hodgkin lymphoma (HL) are believed to derive from germinal center (GC) B cells, but lack expression of a functional B cell receptor. As apoptosis is the normal fate of B-cell receptor-negative GC B cells, mechanisms that abrogate apoptosis are thus critical in HL development, such as epigenetic disruption of certain pro-apoptotic cancer genes including tumor suppressor genes. Identifying methylated genes elucidates oncogenic mechanisms and provides valuable biomarkers; therefore, we performed a chemical epigenetic screening for methylated genes in HL through pharmacological demethylation and expression profiling. IGSF4/CADM1/TSLC1, a pro-apoptotic cell adhesion molecule of the immunoglobulin superfamily, was identified together with other methylated targets. In contrast to its expression in normal GC B cells, IGSF4 was down-regulated and methylated in HL cell lines, most primary HL, and microdissected HRS cells of 3/5 cases, but not in normal peripheral blood mononuclear cells and seldom in normal lymph nodes. We also detected IGSF4 methylation in sera of 14/18 (78%) HL patients but seldom in normal sera. Ectopic IGSF4 expression decreased HL cells survival and increased their sensitivity to apoptosis. IGSF4 induction that normally follows heat shock stress treatment was also abrogated in methylated lymphoma cells. Thus, our data demonstrate that IGSF4 silencing by CpG methylation provides an anti-apoptotic signal to HRS cells important in HL pathogenesis.
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