Article: KRAB zinc finger protein ZNF382 is a proapoptotic tumor suppressor that represses multiple oncogenes and is commonly silenced in multiple carcinomas
| Title | KRAB zinc finger protein ZNF382 is a proapoptotic tumor suppressor that represses multiple oncogenes and is commonly silenced in multiple carcinomas | ||||
|---|---|---|---|---|---|
| Authors | Cheng, Y1 Geng, H1 Cheng, SH5 Liang, P5 Bai, Y4 Li, J1 Srivastava, G2 Ng, MHL5 Fukagawa, T3 Wu, X4 Chan, ATC1 Tao, Q1 | ||||
| Issue Date | 2010 | ||||
| Publisher | American Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/ | ||||
| Citation | Cancer Research, 2010, v. 70 n. 16, p. 6516-6526 [How to Cite?] DOI: http://dx.doi.org/10.1158/0008-5472.CAN-09-4566 | ||||
| Abstract | Zinc finger transcription factors are involved broadly in development and tumorigenesis. Here, we report that the little studied zinc finger transcription factor ZNF382 functions as a tumor suppressor in multiple carcinomas. Although broadly expressed in normal tissues, ZNF382 expression was attenuated in multiple carcinoma cell lines due to promoter CpG methylation. ZNF382 was also frequently methylated in multiple primary tumors (nasopharyngeal, esophageal, colon, gastric, and breast). Ectopic expression of ZNF382 in silenced tumor cells significantly inhibited their clonogenicity and proliferation and induced apoptosis. We further found that ZNF382 inhibited NF-κB and AP-1 signaling and downregulated the expression of multiple oncogenes including MYC, MITF, HMGA2, and CDK6, as well as the NF-κB upstream factors STAT3, STAT5B, ID1, and IKBKE, most likely through heterochromatin silencing. ZNF382 could suppress tumorigenesis through heterochromatin-mediated silencing, as ZNF382 was colocalized and interacted with heterochromatin protein HP1 and further changed the chromatin modifications of ZNF382 target oncogenes. Our data show that ZNF382 is a functional tumor suppressor frequently methylated in multiple carcinomas. ©2010 AACR. | ||||
| ISSN | 0008-5472 2011 Impact Factor: 7.856 2011 SCImago Journal Rankings: 1.309 | ||||
| DOI | http://dx.doi.org/10.1158/0008-5472.CAN-09-4566 | ||||
| ISI Accession Number ID | WOS:000280887000014
Funding Information: Hong Kong RGC grant 474407, Chinese University of Hong Kong Scheme C, and a Chinese University of Hong Kong direct grant. | ||||
| References | References in Scopus |
| dc.contributor.author | Cheng, Y | ||||
|---|---|---|---|---|---|
| dc.contributor.author | Geng, H | ||||
| dc.contributor.author | Cheng, SH | ||||
| dc.contributor.author | Liang, P | ||||
| dc.contributor.author | Bai, Y | ||||
| dc.contributor.author | Li, J | ||||
| dc.contributor.author | Srivastava, G | ||||
| dc.contributor.author | Ng, MHL | ||||
| dc.contributor.author | Fukagawa, T | ||||
| dc.contributor.author | Wu, X | ||||
| dc.contributor.author | Chan, ATC | ||||
| dc.contributor.author | Tao, Q | ||||
| dc.date.accessioned | 2010-12-23T08:38:28Z | ||||
| dc.date.available | 2010-12-23T08:38:28Z | ||||
| dc.date.issued | 2010 | ||||
| dc.description.abstract | Zinc finger transcription factors are involved broadly in development and tumorigenesis. Here, we report that the little studied zinc finger transcription factor ZNF382 functions as a tumor suppressor in multiple carcinomas. Although broadly expressed in normal tissues, ZNF382 expression was attenuated in multiple carcinoma cell lines due to promoter CpG methylation. ZNF382 was also frequently methylated in multiple primary tumors (nasopharyngeal, esophageal, colon, gastric, and breast). Ectopic expression of ZNF382 in silenced tumor cells significantly inhibited their clonogenicity and proliferation and induced apoptosis. We further found that ZNF382 inhibited NF-κB and AP-1 signaling and downregulated the expression of multiple oncogenes including MYC, MITF, HMGA2, and CDK6, as well as the NF-κB upstream factors STAT3, STAT5B, ID1, and IKBKE, most likely through heterochromatin silencing. ZNF382 could suppress tumorigenesis through heterochromatin-mediated silencing, as ZNF382 was colocalized and interacted with heterochromatin protein HP1 and further changed the chromatin modifications of ZNF382 target oncogenes. Our data show that ZNF382 is a functional tumor suppressor frequently methylated in multiple carcinomas. ©2010 AACR. | ||||
| dc.description.nature | Link_to_subscribed_fulltext | ||||
| dc.identifier.citation | Cancer Research, 2010, v. 70 n. 16, p. 6516-6526 [How to Cite?] DOI: http://dx.doi.org/10.1158/0008-5472.CAN-09-4566 | ||||
| dc.identifier.doi | http://dx.doi.org/10.1158/0008-5472.CAN-09-4566 | ||||
| dc.identifier.epage | 6526 | ||||
| dc.identifier.hkuros | 176922 | ||||
| dc.identifier.isi | WOS:000280887000014
Funding Information: Hong Kong RGC grant 474407, Chinese University of Hong Kong Scheme C, and a Chinese University of Hong Kong direct grant. | ||||
| dc.identifier.issn | 0008-5472 2011 Impact Factor: 7.856 2011 SCImago Journal Rankings: 1.309 | ||||
| dc.identifier.issue | 16 | ||||
| dc.identifier.openurl | ![]() | ||||
| dc.identifier.pmid | 20682794 | ||||
| dc.identifier.scopus | eid_2-s2.0-77955728660 | ||||
| dc.identifier.spage | 6516 | ||||
| dc.identifier.uri | http://hdl.handle.net/10722/129528 | ||||
| dc.identifier.volume | 70 | ||||
| dc.language | eng | ||||
| dc.publisher | American Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/ | ||||
| dc.publisher.place | United States | ||||
| dc.relation.ispartof | Cancer Research | ||||
| dc.relation.references | References in Scopus | ||||
| dc.subject.mesh | Animals | ||||
| dc.subject.mesh | DNA-Binding Proteins - biosynthesis - genetics | ||||
| dc.subject.mesh | Genes, Tumor Suppressor | ||||
| dc.subject.mesh | Neoplasms, Multiple Primary - genetics - metabolism - pathology | ||||
| dc.subject.mesh | Transcription Factors - biosynthesis - genetics | ||||
| dc.title | KRAB zinc finger protein ZNF382 is a proapoptotic tumor suppressor that represses multiple oncogenes and is commonly silenced in multiple carcinomas | ||||
| dc.type | Article |
Author Affiliations
- Li Ka Shing Institute of Health Sciences
- The University of Hong Kong
- Sokendai Graduate University for Advanced Studies
- Hunan Normal University
- Chinese University of Hong Kong


