PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Inactivation of parkin by promoter methylation correlated with lymph node metastasis and genomic instability in nasopharyngeal carcinoma.

Abstract This study aimed to investigate the inactivation of the parkin gene by promoter methylation and its relationship with genome instability in nasopharyngeal carcinoma. Parkin was considered as a tumor suppressor gene in various types of cancers. However, its role in nasopharyngeal carcinoma is unexplored. Genomic instabilities were detected in nasopharyngeal carcinoma tissues by the random amplified polymorphic DNA. The methylation-specific polymerase chain reaction, semi-quantitative reverse transcription polymerase chain reaction, and immunohistochemical analysis were used to detect methylation and mRNA and protein expression of parkin in 54 cases of nasopharyngeal carcinoma tissues and 16 cases of normal nasopharyngeal epithelia tissues, and in 5 nasopharyngeal carcinoma cell lines (CNE1, CNE2, TWO3, C666, and HONE1) and 1 normal nasopharyngeal epithelia cell line (NP69). mRNA expression of parkin in CNE1 and CNE2 was analyzed before and after methyltransferase inhibitor 5-aza-2-deoxycytidine treatment. The relationship between promoter methylation and mRNA expression, demethylation and mRNA expression, and mRNA and protein expression of the gene and clinical factors and genomic instabilities were analyzed. The mRNA and protein expression levels were significantly reduced in 54 cases of human nasopharyngeal carcinoma compared with 16 cases of normal nasopharyngeal epithelia. Parkin-methylated cases showed significantly lower mRNA and protein expression levels compared with unmethylated cases. After 5-aza-2-deoxycytidine treatment, parkin mRNA expression was restored in CNE1 and CNE2; 92.59% (50/54) of nasopharyngeal carcinoma demonstrated genomic instability. Parkin is frequently inactivated by promoter methylation, and its mRNA and protein expression correlate with lymph node metastasis and genomic instability. Parkin deficiency probably promotes tumorigenesis in nasopharyngeal carcinoma.
PMID
Related Publications

Inactivation of 14-3-3 sigma by promoter methylation correlates with metastasis in nasopharyngeal carcinoma.

Methylation associated inactivation of RASSF1A and its synergistic effect with activated K-Ras in nasopharyngeal carcinoma.

Silencing of the retinoid response gene TIG1 by promoter hypermethylation in nasopharyngeal carcinoma.

Inactivation of RASSF2A by promoter methylation correlates with lymph node metastasis in nasopharyngeal carcinoma.

Inactivation of PMS2 gene by promoter methylation in nasopharyngeal carcinoma.

Authors

Mayor MeshTerms

Genomic Instability

Keywords

Genome instability

lymph node metastasis

nasopharyngeal carcinoma

parkin gene

promoter methylation

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28351314
OWN - NLM
STAT- MEDLINE
DA  - 20170329
DCOM- 20170407
LR  - 20170407
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 3
DP  - 2017 Mar
TI  - Inactivation of parkin by promoter methylation correlated with lymph node
      metastasis and genomic instability in nasopharyngeal carcinoma.
PG  - 1010428317695025
LID - 10.1177/1010428317695025 [doi]
AB  - This study aimed to investigate the inactivation of the parkin gene by promoter
      methylation and its relationship with genome instability in nasopharyngeal
      carcinoma. Parkin was considered as a tumor suppressor gene in various types of
      cancers. However, its role in nasopharyngeal carcinoma is unexplored. Genomic
      instabilities were detected in nasopharyngeal carcinoma tissues by the random
      amplified polymorphic DNA. The methylation-specific polymerase chain reaction,
      semi-quantitative reverse transcription polymerase chain reaction, and
      immunohistochemical analysis were used to detect methylation and mRNA and protein
      expression of parkin in 54 cases of nasopharyngeal carcinoma tissues and 16 cases
      of normal nasopharyngeal epithelia tissues, and in 5 nasopharyngeal carcinoma
      cell lines (CNE1, CNE2, TWO3, C666, and HONE1) and 1 normal nasopharyngeal
      epithelia cell line (NP69). mRNA expression of parkin in CNE1 and CNE2 was
      analyzed before and after methyltransferase inhibitor 5-aza-2-deoxycytidine
      treatment. The relationship between promoter methylation and mRNA expression,
      demethylation and mRNA expression, and mRNA and protein expression of the gene
      and clinical factors and genomic instabilities were analyzed. The mRNA and
      protein expression levels were significantly reduced in 54 cases of human
      nasopharyngeal carcinoma compared with 16 cases of normal nasopharyngeal
      epithelia. Parkin-methylated cases showed significantly lower mRNA and protein
      expression levels compared with unmethylated cases. After 5-aza-2-deoxycytidine
      treatment, parkin mRNA expression was restored in CNE1 and CNE2; 92.59% (50/54)
      of nasopharyngeal carcinoma demonstrated genomic instability. Parkin is
      frequently inactivated by promoter methylation, and its mRNA and protein
      expression correlate with lymph node metastasis and genomic instability. Parkin
      deficiency probably promotes tumorigenesis in nasopharyngeal carcinoma.
FAU - Ni, Haifeng
AU  - Ni H
AD  - 1 Department of Otolaryngology, Hangzhou First People's Hospital, Nanjing Medical
      University, Hangzhou, China.
FAU - Zhou, Zhen
AU  - Zhou Z
AD  - 1 Department of Otolaryngology, Hangzhou First People's Hospital, Nanjing Medical
      University, Hangzhou, China.
FAU - Jiang, Bo
AU  - Jiang B
AD  - 1 Department of Otolaryngology, Hangzhou First People's Hospital, Nanjing Medical
      University, Hangzhou, China.
FAU - Yuan, Xiaoyang
AU  - Yuan X
AD  - 1 Department of Otolaryngology, Hangzhou First People's Hospital, Nanjing Medical
      University, Hangzhou, China.
FAU - Cao, Xiaolin
AU  - Cao X
AD  - 1 Department of Otolaryngology, Hangzhou First People's Hospital, Nanjing Medical
      University, Hangzhou, China.
FAU - Huang, Guangwu
AU  - Huang G
AD  - 2 Department of Otolaryngology, First Affiliated Hospital, Guangxi Medical
      University, Nanning, China.
FAU - Li, Yong
AU  - Li Y
AD  - 1 Department of Otolaryngology, Hangzhou First People's Hospital, Nanjing Medical
      University, Hangzhou, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.3.2.27 (parkin protein)
RN  - Nasopharyngeal carcinoma
SB  - IM
MH  - Adult
MH  - Aged
MH  - Carcinogenesis/genetics
MH  - Cell Line, Tumor
MH  - DNA Methylation/*genetics
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - *Genomic Instability
MH  - Humans
MH  - Lymphatic Metastasis/genetics/pathology
MH  - Male
MH  - Middle Aged
MH  - Nasopharyngeal Neoplasms/*genetics/pathology
MH  - Promoter Regions, Genetic
MH  - Ubiquitin-Protein Ligases/antagonists & inhibitors/biosynthesis/*genetics
OTO - NOTNLM
OT  - Genome instability
OT  - lymph node metastasis
OT  - nasopharyngeal carcinoma
OT  - parkin gene
OT  - promoter methylation
EDAT- 2017/03/30 06:00
MHDA- 2017/04/08 06:00
CRDT- 2017/03/30 06:00
AID - 10.1177/1010428317695025 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Mar;39(3):1010428317695025. doi: 10.1177/1010428317695025.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>