PMID- 25556465
OWN - NLM
STAT- MEDLINE
DCOM- 20150909
LR  - 20190606
IS  - 2476-762X (Electronic)
IS  - 1513-7368 (Linking)
VI  - 15
IP  - 23
DP  - 2014
TI  - Epigenetic changes within the promoter regions of antigen processing machinery 
      family genes in Kazakh primary esophageal squamous cell carcinoma.
PG  - 10299-306
AB  - The esophageal squamous cell carcinoma (ESCC) is thought to develop through a 
      multi-stage process. Epigenetic gene silencing constitutes an alternative or 
      complementary mechanism to mutational events in tumorigenesis. 
      Posttranscriptional regulation of human leukocyte antigen class I (HLA-I) and 
      antigen processing machinery (APM) proteins expression may be associated with 
      novel epigenetic modifications in cancer development. In the present study, we 
      determined the expression levels of HLA-I antigen and APM components by 
      immunohistochemistry. Then by a bisulfite-sequencing PCR (BSP) approach, we 
      identified target CpG islands methylated at the gene promoter region of APM 
      family genes in a ESCC cell line (ECa109), and further quantitative analysis of 
      CpG site specific methylation of these genes in cases of Kazakh primary ESCCs 
      with corresponding non-cancerous esophageal tissues using the Sequenom MassARRAY 
      platform. Here we showed that the development of ESCCs was accompanied by partial 
      or total loss of protein expression of HLA-B, TAP2, LMP7, tapasin and ERp57. The 
      results demonstrated that although no statistical significance was found of 
      global target CpG fragment methylation level sof HLA-B, TAP2, tapasin and ERp57 
      genes between ESCC and corresponding non-cancerous esophageal tissues, there was 
      significant differences in the methylation level of several single sites between 
      the two groups. Of thesse only the global methylation level of LMP7 gene target 
      fragments was statistically higher (0.0517+/-0.0357) in Kazakh esophageal cancer 
      than in neighboring normal tissues (0.0380+/-0.0214, p<0.05). Our results suggest 
      that multiple CpG sites, but not methylation of every site leads to down 
      regulation or deletion of gene expression. Only some of them result in genetic 
      transcription, and silencing of HLA-B, ERp57, and LMP7 expression through 
      hypermethylation of the promoters or other mechanisms may contribute to 
      mechanisms of tumor escape from immune surveillance in Kazakh esophageal 
      carcinogenesis.
FAU - Sheyhidin, Ilyar
AU  - Sheyhidin I
AD  - Department of Thoracic Surgery, the First Affliated Hospital, Medical University 
      of Xinjiang, Urumqi, China E-mail : axiangu75@126.com.
FAU - Hasim, Ayshamgul
AU  - Hasim A
FAU - Zheng, Feng
AU  - Zheng F
FAU - Ma, Hong
AU  - Ma H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Thailand
TA  - Asian Pac J Cancer Prev
JT  - Asian Pacific journal of cancer prevention : APJCP
JID - 101130625
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 3)
RN  - 0 (ATP-Binding Cassette Transporters)
RN  - 0 (HLA-B Antigens)
RN  - 0 (Membrane Transport Proteins)
RN  - 0 (tapasin)
RN  - 145892-13-3 (TAP2 protein, human)
RN  - EC 3.4.25.1 (LMP7 protein)
RN  - EC 3.4.25.1 (Proteasome Endopeptidase Complex)
RN  - EC 5.3.4.1 (Protein Disulfide-Isomerases)
RN  - EC 5.3.4.1. (PDIA3 protein, human)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 3
MH  - ATP-Binding Cassette Transporters/genetics
MH  - Adult
MH  - Aged
MH  - Antigen Presentation/*genetics
MH  - Carcinoma, Squamous Cell/*genetics
MH  - Case-Control Studies
MH  - Cell Line, Tumor
MH  - CpG Islands
MH  - DNA Methylation
MH  - Epigenesis, Genetic
MH  - Esophageal Neoplasms/*genetics
MH  - Esophageal Squamous Cell Carcinoma
MH  - Esophagus/metabolism
MH  - Female
MH  - *Gene Expression Regulation, Neoplastic
MH  - Genes, MHC Class I/*genetics
MH  - HLA-B Antigens/genetics
MH  - Humans
MH  - Kazakhstan
MH  - Male
MH  - Membrane Transport Proteins/genetics
MH  - Middle Aged
MH  - Promoter Regions, Genetic
MH  - Proteasome Endopeptidase Complex/genetics
MH  - Protein Disulfide-Isomerases/genetics
MH  - Tumor Escape/genetics
EDAT- 2015/01/06 06:00
MHDA- 2015/09/10 06:00
CRDT- 2015/01/06 06:00
PHST- 2015/01/06 06:00 [entrez]
PHST- 2015/01/06 06:00 [pubmed]
PHST- 2015/09/10 06:00 [medline]
AID - 10.7314/apjcp.2014.15.23.10299 [doi]
PST - ppublish
SO  - Asian Pac J Cancer Prev. 2014;15(23):10299-306. doi: 
      10.7314/apjcp.2014.15.23.10299.