PMID- 16142337
OWN - NLM
STAT- MEDLINE
DCOM- 20060203
LR  - 20151119
IS  - 1021-335X (Print)
IS  - 1021-335X (Linking)
VI  - 14
IP  - 4
DP  - 2005 Oct
TI  - Frequent hemizygous deletion at 1p36 and hypermethylation downregulate RUNX3 
      expression in human lung cancer cell lines.
PG  - 817-22
AB  - Runt-related transcription factor 3 (RUNX3) has been recognized as a tumor 
      suppressor gene in gastric cancer because its expression level was reduced or 
      disappeared due to epigenetic changes. To evaluate the usefulness of the RUNX3 
      gene as a biomarker of lung cancer, we have analyzed the expression of the RUNX3 
      gene in 15 lung cancer cell lines by real-time reverse transcription-polymerase 
      chain reaction (RT-PCR), and demonstrated that RUNX3 gene expression was reduced 
      or disappeared in all cell lines examined (100%). In addition, we have attempted 
      to classify all the cell lines into three groups according to the expression 
      level; less than 10% (group I), 10-30% (group II) and approximately 50% (group 
      III). We further investigated methylation status of the CpG sites in the exon 1 
      region of RUNX3 by methylation specific PCR (MSP), and studied the correlation 
      between the expression level and hemizygous deletion as revealed by bicolor 
      fluorescence in situ hybridization (FISH). The CpG sites were hypermethylated in 
      8 cell lines (53%) and the RUNX3 loci were hemizygously deleted in another 8 cell 
      lines (53%). Furthermore group I, II, and III corresponded well to 
      methylation-positive cell lines, cell lines showing hemizygous deletion, and the 
      rest of cell lines without methylation or hemizygous deletion, respectively. 
      These results suggest that a comprehensive study on RUNX3 using real-time RT-PCR, 
      MSP, and FISH could be beneficial in understanding the pathogenetic mechanisms of 
      human lung cancer at the molecular level.
FAU - Yanada, Masashi
AU  - Yanada M
AD  - Department of Cardiovascular and Thoracic Surgery, Graduate School of Medical 
      Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho, 
      Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan.
FAU - Yaoi, Takeshi
AU  - Yaoi T
FAU - Shimada, Junichi
AU  - Shimada J
FAU - Sakakura, Chouhei
AU  - Sakakura C
FAU - Nishimura, Motohiro
AU  - Nishimura M
FAU - Ito, Kazuhiro
AU  - Ito K
FAU - Terauchi, Kunihiko
AU  - Terauchi K
FAU - Nishiyama, Katsuhiko
AU  - Nishiyama K
FAU - Itoh, Kyoko
AU  - Itoh K
FAU - Fushiki, Shinji
AU  - Fushiki S
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (Antimetabolites, Antineoplastic)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Core Binding Factor Alpha 3 Subunit)
RN  - 0 (DNA, Complementary)
RN  - 0 (Hydroxamic Acids)
RN  - 0 (Protein Synthesis Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 3X2S926L3Z (trichostatin A)
RN  - M801H13NRU (Azacitidine)
SB  - IM
MH  - Alleles
MH  - Antimetabolites, Antineoplastic/pharmacology
MH  - Azacitidine/pharmacology
MH  - Biomarkers, Tumor
MH  - Cell Line, Tumor
MH  - Chromosomes, Human, Pair 1/*genetics
MH  - Core Binding Factor Alpha 3 Subunit/*genetics
MH  - CpG Islands
MH  - *DNA Methylation
MH  - DNA, Complementary/metabolism
MH  - *Down-Regulation
MH  - Exons
MH  - *Gene Deletion
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Hydroxamic Acids/pharmacology
MH  - In Situ Hybridization, Fluorescence
MH  - Lung Neoplasms/*genetics
MH  - Polymerase Chain Reaction
MH  - Protein Synthesis Inhibitors/pharmacology
MH  - RNA, Messenger/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2005/09/06 09:00
MHDA- 2006/02/04 09:00
CRDT- 2005/09/06 09:00
PHST- 2005/09/06 09:00 [pubmed]
PHST- 2006/02/04 09:00 [medline]
PHST- 2005/09/06 09:00 [entrez]
PST - ppublish
SO  - Oncol Rep. 2005 Oct;14(4):817-22.