title: Methylation of PRDM2, PRDM5 and PRDM16 genes in lung cancer cells.
abstract: OBJECTIVE
  To investigate the changes of expression and methylation status of PRDM2, PRDM5, PRDM16 in lung cancer cells after treatment with demethylation agent.
  
  
  METHODS
  A549 (lung adenocarcinoma cell line), HTB-182 (lung squamous cell carcinoma cell line) and HBE (normal bronchial cell line) were treated with 5-aza-2dC. The methylation state of PRDM2, PRDM5, PRDM16 was detected by MSP. The expression of PRDM2, PRDM5, PRDM16 was detected by RT-PCR and Western blot analysis. Cell growth was detected by MTT assay.
  
  
  RESULTS
  5-aza-2-dC reduced the methylation of PRDM2, PRDM5, PRDM16 gene in A549 and HTB-182 cells but not in HBE cells. Consistently, 5-aza-2dC increased mRNA and protein expression of PRDM2, PRDM5, PRDM16 in A549 and HTB-182 cells but not in HBE cells. Furthermore, 5-aza-2dC inhibited the growth of A549 and HTB-182 cells but not HBE cells.
  
  
  CONCLUSIONS
  PRDM2, PRDM5, PRDM16 promoters are methylated and their expression is suppressed in lung cancer cells. Demethylation drug 5-aza-2dC could upregulate the expression of PRDM2, PRDM5, PRDM16 and suppress lung cancer cell growth. 5-aza-2dC has potential to be used for lung cancer therapy by epigenetic mechanism.
authors: Clinical Laboratory, Xiangya Hospital, Central South University Changsha, China.
authors: Shuang-Xiang
authors: SX
authors: Tan
authors: Hunan Province Geriatric Hospital Changsha, China.
authors: Rui-Cheng
authors: RC
authors: Hu
authors: Hunan Province Geriatric Hospital Changsha, China.
authors: Jing-Jing
authors: JJ
authors: Liu
authors: Hunan Province Geriatric Hospital Changsha, China.
authors: Yong-Li
authors: YL
authors: Tan
authors: Clinical Laboratory, Xiangya Hospital, Central South University Changsha, China.
authors: Wen-En
authors: WE
authors: Liu
mesh_terms: D001374:Azacitidine / Q000031:analogs & derivatives / Q000494:pharmacology; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D019175:DNA Methylation / Q000187:drug effects; D015254:DNA Modification Methylases / Q000037:antagonists & inhibitors / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D000077209:Decitabine; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D044127:Epigenesis, Genetic / Q000187:drug effects; D015972:Gene Expression Regulation, Neoplastic; D011495:Histone-Lysine N-Methyltransferase / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics* / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics* / Q000378:metabolism; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000378:metabolism; D013997:Time Factors; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism
chemical_list: D004268:DNA-Binding Proteins; D004791:Enzyme Inhibitors; D009687:Nuclear Proteins; C416371:PRDM16 protein, human; C487762:PRDM5 protein, human; D012333:RNA, Messenger; D014157:Transcription Factors; D000077209:Decitabine; D015254:DNA Modification Methylases; D011495:Histone-Lysine N-Methyltransferase; C093563:PRDM2 protein, human; D001374:Azacitidine
keywords: PRDM; epigenetics; gene expression; lung cancer; methylation