PMID- 21636313
OWN - NLM
STAT- MEDLINE
DCOM- 20110913
LR  - 20140731
IS  - 1879-0593 (Electronic)
IS  - 1368-8375 (Linking)
VI  - 47
IP  - 7
DP  - 2011 Jul
TI  - The involvement of CHD5 hypermethylation in laryngeal squamous cell carcinoma.
PG  - 601-8
LID - 10.1016/j.oraloncology.2011.05.003 [doi]
AB  - Chromodomain helicase DNA-binding protein 5 (CHD5) has been found to be a 
      candidate tumor suppressor gene (TSG) in malignant neural tumors. In mice 
      heterozygous for chd5 deficiency, the first tumor observed was pathological 
      squamous cell carcinoma. More than 95% of primary laryngeal cancer is squamous 
      cell carcinoma. Thus, we explored the expression of CHD5 in 65 patients with 
      laryngeal squamous cell carcinoma (LSCC) using real-time PCR, 
      immunohistochemistry and Western blotting. DNA methylation was detected using 
      bisulfate-specific sequencing. The potential function of CHD5 was determined 
      using MTT, apoptosis and transwell migration assays in CHD5-transfected Hep-2 
      cells. Our results revealed that the mRNA and protein expression levels of CHD5 
      in LSCC tissues were significantly lower than those in clear surgical margin 
      tissues (p<0.05), and there is a significant correlation between the mRNA and 
      protein expression levels of CHD5 (p<0.01). In addition, there were significant 
      differences in CHD5 mRNA and protein levels with respect to the patient's 
      clinical stage (p<0.05). Aberrant methylation of the CHD5 promoter was frequently 
      found in the Hep-2 cell line and LSCC tumor tissues, especially tumor tissues 
      from advanced TNM (p<0.05) or older patients (p<0.05). Finally, ectopic 
      expression of CHD5 in laryngeal cancer cells led to significant inhibition of 
      growth and invasiveness. Our data suggest that CHD5 is a tumor suppressor gene 
      that is epigenetically downregulated in LSCC.
CI  - Copyright (c) 2011 Elsevier Ltd. All rights reserved.
FAU - Wang, Jin
AU  - Wang J
AD  - Department of Medical Genetics, China Medical University, 92 Beier Road, Heping 
      District, Shenyang 110001, PR China.
FAU - Chen, Hong
AU  - Chen H
FAU - Fu, Shuang
AU  - Fu S
FAU - Xu, Zhen-Ming
AU  - Xu ZM
FAU - Sun, Kai-Lai
AU  - Sun KL
FAU - Fu, Wei-Neng
AU  - Fu WN
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110601
PL  - England
TA  - Oral Oncol
JT  - Oral oncology
JID - 9709118
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - EC 3.6.4.- (DNA Helicases)
RN  - EC 3.6.4.12 (CHD5 protein, human)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Carcinoma, Squamous Cell/*genetics/metabolism
MH  - Cell Line, Tumor
MH  - DNA Helicases/*genetics
MH  - DNA Methylation
MH  - Down-Regulation
MH  - Female
MH  - Gene Expression Regulation, Neoplastic/genetics
MH  - *Genes, Tumor Suppressor
MH  - Humans
MH  - Laryngeal Neoplasms/*genetics/metabolism
MH  - Male
MH  - Mice
MH  - Middle Aged
MH  - Neoplasm Proteins/*genetics/metabolism
MH  - Nerve Tissue Proteins/*genetics
MH  - Promoter Regions, Genetic
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2011/06/04 06:00
MHDA- 2011/09/14 06:00
CRDT- 2011/06/04 06:00
PHST- 2011/01/03 00:00 [received]
PHST- 2011/05/02 00:00 [revised]
PHST- 2011/05/07 00:00 [accepted]
PHST- 2011/06/04 06:00 [entrez]
PHST- 2011/06/04 06:00 [pubmed]
PHST- 2011/09/14 06:00 [medline]
AID - S1368-8375(11)00167-9 [pii]
AID - 10.1016/j.oraloncology.2011.05.003 [doi]
PST - ppublish
SO  - Oral Oncol. 2011 Jul;47(7):601-8. doi: 10.1016/j.oraloncology.2011.05.003. Epub 
      2011 Jun 1.