ArticleInternational journal of molecular medicine2015
5-Azacitidine induces demethylation of PTPL1 and inhibits growth in non-Hodgkin lymphoma.
Article in International journal of molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- 5‑Aza‑dC suppresses melanoma progression by inhibiting GAS5 hypermethylation.Oncology reports · 2022Article
- Low-Dose 5-Aza and DZnep Alleviate Acute Graft-Frontiers in immunology · 2022Article
- ARID1A genomic alterations driving microsatellite instability through somatic MLH1 methylation with response to immunotherapy in metastatic lung adenocarcinoma: a case report.Journal of medical case reports · 2021Article
- Dual Role of the PTPN13 Tyrosine Phosphatase in Cancer.Biomolecules · 2020Review
- Molecular Subtyping in Diffuse Large B Cell Lymphoma: Closer to an Approach of Precision Therapy.Current treatment options in oncology · 2017Review
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
Non-Hodgkin lymphoma (NHL) consists of various lymphoid malignancies with a diverse clinical pathology and biological characteristics. Methylation of cytosine residues by DNA methyltransferases at CpG dinucleotides in the promoter region of the genes is a major epigenetic modification in mammalian genomes that can have profound effects on gene expression. The PTPL1 methylation pattern was screened by methylation‑specific polymerase chain reaction (MSP) in 7 lymphoma‑derived cell lines and in 47 samples of diffuse large B cell lymphoma (DLBCL). The PTPL1 gene was hypermethylated in the CA46, Raji, Jurkat and DB cell lines; however, it was unmethylated in the Hut78, Maver and Z138 cell lines. The expression of PTPL1 mRNA was re‑inducible by 5‑azacytidine (5‑Aza), an agent of DNA demethylation. The methylations were detected in 59.6% of DLBCL versus 6.3% in reactive lymph node proliferation. Therefore, the present data showed that PTPL1 was epigenetically regulated in NHL suggesting an involvement of the PTPL1 tumor‑suppressor genes in NHL, and highlights 5-Aza as a potential therapeutic candidate for NHL.
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