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- Publisher Website: 10.1038/sj.onc.1209767
- Scopus: eid_2-s2.0-33846046177
- PMID: 16799631
- WOS: WOS:000243236500015
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Article: Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9
Title | Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9 |
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Authors | |
Keywords | ADAMTS9 Chromosome 3 Esophageal carcinoma Microcell-mediated chromosome transfer Tumor suppressor gene |
Issue Date | 2007 |
Publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/onc |
Citation | Oncogene, 2007, v. 26 n. 1, p. 148-157 How to Cite? |
Abstract | A gene critical to esophageal cancer has been identified. Functional studies using microcell-mediated chromosome transfer of intact and truncated donor chromosomes 3 into an esophageal cancer cell line and nude mouse tumorigenicity assays were used to identify a 1.61 Mb tumor suppressive critical region (CR) mapping to chromosome 3p14.2. This CR is bounded by D3S1600 and D3S1285 microsatellite markers. One candidate tumor suppressor gene, ADAMTS9, maps to this CR. Further studies showed normal expression levels of this gene in tumor-suppressed microcell hybrids, levels that were much higher than observed in the recipient cells. Complete loss or downregulation of ADAMTS9 gene expression was found in 15 out of 16 esophageal carcinoma cell lines. Promoter hypermethylation was detected in the cell lines that do not express this gene. Re-expression of ADAMTS9 was observed after demethylation drug treatment, confirming that hypermethylation is involved in gene downregulation. Downregulation of ADAMTS9 was also found in 43.5 and 47.6% of primary esophageal tumor tissues from Hong Kong and from the high-risk region of Henan, respectively. Thus, this study identifies and provides functional evidence for a CR associated with tumor suppression on 3p14.2 and provides the first evidence that ADAMTS9, mapping to this region, may contribute to esophageal cancer development. © 2007 Nature Publishing Group All rights reserved. |
Persistent Identifier | http://hdl.handle.net/10722/148498 |
ISSN | 2023 Impact Factor: 6.9 2023 SCImago Journal Rankings: 2.334 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lo, PHY | en_HK |
dc.contributor.author | Leung, ACC | en_HK |
dc.contributor.author | Kwok, CYC | en_HK |
dc.contributor.author | Cheung, WSY | en_HK |
dc.contributor.author | Ko, JMY | en_HK |
dc.contributor.author | Yang, LC | en_HK |
dc.contributor.author | Law, S | en_HK |
dc.contributor.author | Wang, LD | en_HK |
dc.contributor.author | Li, J | en_HK |
dc.contributor.author | Stanbridge, EJ | en_HK |
dc.contributor.author | Srivastava, G | en_HK |
dc.contributor.author | Tang, JCO | en_HK |
dc.contributor.author | Tsao, SW | en_HK |
dc.contributor.author | Lung, ML | en_HK |
dc.date.accessioned | 2012-05-29T06:13:19Z | - |
dc.date.available | 2012-05-29T06:13:19Z | - |
dc.date.issued | 2007 | en_HK |
dc.identifier.citation | Oncogene, 2007, v. 26 n. 1, p. 148-157 | en_HK |
dc.identifier.issn | 0950-9232 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/148498 | - |
dc.description.abstract | A gene critical to esophageal cancer has been identified. Functional studies using microcell-mediated chromosome transfer of intact and truncated donor chromosomes 3 into an esophageal cancer cell line and nude mouse tumorigenicity assays were used to identify a 1.61 Mb tumor suppressive critical region (CR) mapping to chromosome 3p14.2. This CR is bounded by D3S1600 and D3S1285 microsatellite markers. One candidate tumor suppressor gene, ADAMTS9, maps to this CR. Further studies showed normal expression levels of this gene in tumor-suppressed microcell hybrids, levels that were much higher than observed in the recipient cells. Complete loss or downregulation of ADAMTS9 gene expression was found in 15 out of 16 esophageal carcinoma cell lines. Promoter hypermethylation was detected in the cell lines that do not express this gene. Re-expression of ADAMTS9 was observed after demethylation drug treatment, confirming that hypermethylation is involved in gene downregulation. Downregulation of ADAMTS9 was also found in 43.5 and 47.6% of primary esophageal tumor tissues from Hong Kong and from the high-risk region of Henan, respectively. Thus, this study identifies and provides functional evidence for a CR associated with tumor suppression on 3p14.2 and provides the first evidence that ADAMTS9, mapping to this region, may contribute to esophageal cancer development. © 2007 Nature Publishing Group All rights reserved. | en_HK |
dc.language | eng | en_US |
dc.publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/onc | en_HK |
dc.relation.ispartof | Oncogene | en_HK |
dc.subject | ADAMTS9 | en_HK |
dc.subject | Chromosome 3 | en_HK |
dc.subject | Esophageal carcinoma | en_HK |
dc.subject | Microcell-mediated chromosome transfer | en_HK |
dc.subject | Tumor suppressor gene | en_HK |
dc.subject.mesh | Adam Proteins - Genetics | en_US |
dc.subject.mesh | Base Sequence | en_US |
dc.subject.mesh | Carcinoma, Squamous Cell - Genetics | en_US |
dc.subject.mesh | Chromosome Mapping | en_US |
dc.subject.mesh | Chromosomes, Human, Pair 3 | en_US |
dc.subject.mesh | Dna | en_US |
dc.subject.mesh | Dna Methylation | en_US |
dc.subject.mesh | Esophageal Neoplasms - Genetics | en_US |
dc.subject.mesh | Gene Expression Regulation, Neoplastic | en_US |
dc.subject.mesh | Genes, Tumor Suppressor | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | In Situ Hybridization, Fluorescence | en_US |
dc.subject.mesh | Molecular Sequence Data | en_US |
dc.title | Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9 | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Law, S:slaw@hku.hk | en_HK |
dc.identifier.email | Srivastava, G:gopesh@pathology.hku.hk | en_HK |
dc.identifier.email | Tsao, SW:gswtsao@hkucc.hku.hk | en_HK |
dc.identifier.email | Lung, ML:mlilung@hku.hk | en_HK |
dc.identifier.authority | Law, S=rp00437 | en_HK |
dc.identifier.authority | Srivastava, G=rp00365 | en_HK |
dc.identifier.authority | Tsao, SW=rp00399 | en_HK |
dc.identifier.authority | Lung, ML=rp00300 | en_HK |
dc.description.nature | link_to_OA_fulltext | en_US |
dc.identifier.doi | 10.1038/sj.onc.1209767 | en_HK |
dc.identifier.pmid | 16799631 | - |
dc.identifier.scopus | eid_2-s2.0-33846046177 | en_HK |
dc.identifier.hkuros | 140863 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-33846046177&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 26 | en_HK |
dc.identifier.issue | 1 | en_HK |
dc.identifier.spage | 148 | en_HK |
dc.identifier.epage | 157 | en_HK |
dc.identifier.isi | WOS:000243236500015 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Lo, PHY=36762664000 | en_HK |
dc.identifier.scopusauthorid | Leung, ACC=15760220500 | en_HK |
dc.identifier.scopusauthorid | Kwok, CYC=15760014400 | en_HK |
dc.identifier.scopusauthorid | Cheung, WSY=15759017200 | en_HK |
dc.identifier.scopusauthorid | Ko, JMY=35725559400 | en_HK |
dc.identifier.scopusauthorid | Yang, LC=7406280398 | en_HK |
dc.identifier.scopusauthorid | Law, S=7202241293 | en_HK |
dc.identifier.scopusauthorid | Wang, LD=12242861000 | en_HK |
dc.identifier.scopusauthorid | Li, J=27168754300 | en_HK |
dc.identifier.scopusauthorid | Stanbridge, EJ=7103249410 | en_HK |
dc.identifier.scopusauthorid | Srivastava, G=7202242238 | en_HK |
dc.identifier.scopusauthorid | Tang, JCO=14056850300 | en_HK |
dc.identifier.scopusauthorid | Tsao, SW=7102813116 | en_HK |
dc.identifier.scopusauthorid | Lung, ML=7006411788 | en_HK |
dc.identifier.citeulike | 714396 | - |
dc.identifier.issnl | 0950-9232 | - |