IR@PKUHSC  > 北京大学第三临床医学院  > 血液内科
学科主题临床医学
Promoter hypermethylation of PTPL1, PTPN6, DAPK, p16 and 5-azacitidine inhibits growth in DLBCL
Wang, Wenming1; Wang, Jing1; Li, Zhengqian2; Zhu, Mingxia1; Zhang, Zhe3; Wang, Yanfang1; Jing, Hongmei1
关键词protein tyrosine phosphatase 1 PTPN6 DAPK p16 diffuse large B cell lymphoma methylation 5-azacitidine
刊名ONCOLOGY REPORTS
2016
DOI10.3892/or.2015.4347
35期:1页:139-146
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
研究领域[WOS]Oncology
关键词[WOS]B-CELL LYMPHOMA ; EPIGENETIC THERAPY ; GENE-EXPRESSION ; DNA METHYLATION ; CANCER ; PROLIFERATION ; APOPTOSIS ; DNMT3B ; BAX
英文摘要

Aberrant hypermethylation of CpG islands of tumor suppressor is one of the mechanisms for epigenetic loss of gene function. In the present study, the methylation status of the promoter regions of protein tyrosine phosphatase (PTPN) 6, DAPK, and p16 were studied using methylation-specific polymerase chain reaction (MSP) in 26 diffuse large B cell lymphoma (DLBCL) lymphomas. In OCI-LY1 cell line, gene methylation status, expression of PTPL1 and its reactivation by DNA demethylation was determined by PCR and on the protein level by western blotting. ELISA-like reaction was used to detect global DNA methylation measurement. Induction of apoptosis by 5-azacitidine was analyzed by Annexin V/PI staining and flow cytometry. Our results show that hypermethylation of the PTPN6 gene promoter region was found in 15.4% (4/26), the DAPK gene promoter region in 30.8% (8/26), the p16 gene promoter region in 7.7% (2/26). Notably, we identified that PTPL1 was hypermethylated and transcriptionally silenced in OCI-LY1 cell line. The expression of PTPL1 was re-inducible by 5-azacytidine. 5-azacytidine also inhibits the proliferation and decreases the global methylation level of the OCI-LY1 cell line. We can conclude from our study that a higher prevalence of methylation of PTPL1, PTPN6, DAPK and p16 occur in DLBCL. Our data also highlights 5-azacytidine as a potential therapeutic candidate for DLBCL. Further studies are required to substantiate the role of methylation of PTPL1, PTPN6, DAPK and p16 as a marker in diffuse large B cell lymphoma.

语种英语
WOS记录号WOS:000366072500016
Citation statistics
Cited Times:1[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/66432
Collection北京大学第三临床医学院_血液内科
作者单位1.Peking Univ, Dept Hematol, Hosp 3, Beijing 100191, Peoples R China
2.Peking Univ, Dept Anesthesiol, Hosp 3, Beijing 100191, Peoples R China
3.Peking Univ, Dept Urol, Hosp 3, Beijing 100191, Peoples R China
Recommended Citation
GB/T 7714
Wang, Wenming,Wang, Jing,Li, Zhengqian,et al. Promoter hypermethylation of PTPL1, PTPN6, DAPK, p16 and 5-azacitidine inhibits growth in DLBCL[J]. ONCOLOGY REPORTS,2016,35(1):139-146.
APA Wang, Wenming.,Wang, Jing.,Li, Zhengqian.,Zhu, Mingxia.,Zhang, Zhe.,...&Jing, Hongmei.(2016).Promoter hypermethylation of PTPL1, PTPN6, DAPK, p16 and 5-azacitidine inhibits growth in DLBCL.ONCOLOGY REPORTS,35(1),139-146.
MLA Wang, Wenming,et al."Promoter hypermethylation of PTPL1, PTPN6, DAPK, p16 and 5-azacitidine inhibits growth in DLBCL".ONCOLOGY REPORTS 35.1(2016):139-146.
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