Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/34908
Title: Monochromosome transfer and microarray analysis identify a critical tumor-suppressive region mapping to chromosome 13q14 and THSD1 in esophageal carcinoma
Authors: Ko, JM
Chan, PL
Yau, WL
Chan, HK
Chan, KC
Yu, ZY
Kwong, FM
Miller, LD
Liu, ET
Yang, LC
Lo, PHY
Stanbridge, EJ
Tang, JCO 
Srivastava, G
Tsao, SW
Law, S
Lung, ML
Keywords: THSD1
ESCC
13q14
TSG
Hypermethylation
Issue Date: 2008
Publisher: American Association for Cancer Research
Source: Molecular cancer research, 2008, v. 6, no. 4, p. 592-603 How to cite?
Journal: Molecular cancer research
Abstract: Loss of chromosome 13q regions in esophageal squamous cell carcinoma (ESCC) is a frequent event. Monochromosome transfer approaches provide direct functional evidence for tumor suppression by chromosome 13 in SLMT-1, an ESCC cell line, and identify critical regions at 13q12.3, 13q14.11, and 13q14.3. Differential gene expression profiles of three tumor-suppressing microcell hybrids (MCH) and their tumorigenic parental SLMT-1 cell line were revealed by competitive hybridization using 19k cDNA oligonucleotide microarrays. Nine candidate 13q14 tumor-suppressor genes (TSG), including RB1, showed down-regulation in SLMT-1, compared with NE1, an immortalized normal esophageal epithelial cell line; their average gene expression was restored in MCHs compared with SLMT-1. Reverse transcription-PCR validated gene expression levels in MCHs and a panel of ESCC cell lines. Results suggest that the tumor-suppressing effect is not attributed to RB1, but instead likely involves thrombospondin type I domain-containing 1 (THSD1), a novel candidate TSG mapping to 13q14. Quantitative reverse transcription-PCR detected down-regulation of THSD1 expression in 100% of ESCC and other cancer cell lines. Mechanisms for THSD1 silencing in ESCC involved loss of heterozygosity and promoter hypermethylation, as analyzed by methylation-specific PCR and clonal bisulfite sequencing. Transfection of wild-type THSD1 into SLMT-1 resulted in significant reduction of colony-forming ability, hence providing functional evidence for its growth-suppressive activity. These findings suggest that THSD1 is a good candidate TSG. (Mol Cancer Res 2008;6(4):592–603)
URI: http://hdl.handle.net/10397/34908
ISSN: 1541-7786 (print)
1557-3125 (online)
DOI: 10.1158/1541-7786.MCR-07-0154
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