Article: miR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion
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- Publisher Website: 10.1016/j.bbrc.2009.11.093
- Scopus: eid_2-s2.0-72949119530
- PMID: 19931509
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| Title | miR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion | ||||||
|---|---|---|---|---|---|---|---|
| Authors | Xia, H2 Ng, SS2 Jiang, S3 Cheung, WKC2 Sze, J2 Bian, XW4 Kung, Hf1 3 Lin, MC2 | ||||||
| Keywords | β-catenin Invasion microRNA Migration Nasopharyngeal carcinoma | ||||||
| Issue Date | 2010 | ||||||
| Publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description | ||||||
| Citation | Biochemical And Biophysical Research Communications, 2010, v. 391 n. 1, p. 535-541 [How to Cite?] DOI: http://dx.doi.org/10.1016/j.bbrc.2009.11.093 | ||||||
| Abstract | Nasopharyngeal carcinoma (NPC), a highly metastatic and invasive malignant tumor originating from the nasopharynx, is widely prevalent in Southeast Asia, the Middle East and North Africa. Although viral, dietary and genetic factors have been implicated in NPC, the molecular basis of its pathogenesis is not well defined. Based on a recent microRNA (miRNA) microarray study showing miR-200 downregulation in NPC, we further investigated the role of miR-200a in NPC carcinogenesis. We found that the endogenous miR-200a expression level increases with the degree of differentiation in a panel of NPC cell lines, namely undifferentiated C666-1, high-differentiated CNE-1, and low-differentiated CNE-2 and HNE1 cells. By a series of gain-of-function and loss-of-function studies, we showed that over-expression of miR-200a inhibits C666-1 cell growth, migration and invasion, whereas its knock-down stimulates these processes in CNE-1 cells. In addition, we further identified ZEB2 and CTNNB1 as the functional downstream targets of miR-200a. Interestingly, knock-down of ZEB2 solely impeded NPC cell migration and invasion, whereas CTNNB1 suppression only inhibited NPC cell growth, suggesting that the inhibitory effects of miR-200a on NPC cell growth, migration and invasion are mediated by distinct targets and pathways. Our results reveal the important role of miR-200a as a regulatory factor of NPC carcinogenesis and a potential candidate for miRNA-based therapy against NPC. © 2009 Elsevier Inc. All rights reserved. | ||||||
| ISSN | 0006-291X 2011 Impact Factor: 2.484 2011 SCImago Journal Rankings: 0.287 | ||||||
| DOI | http://dx.doi.org/10.1016/j.bbrc.2009.11.093 | ||||||
| ISI Accession Number ID | WOS:000273624500094
Funding Information: We thank Mr. Wesley Tucker for critical reading of the paper. This work was Supported by the Research Grants Council of the Hong Kong Special Administrative Region, China (No. 467109). National Basic Research Program of China (973 Program) (Nos. 2010CB529400; 2010CB912800). | ||||||
| References | References in Scopus |
| dc.contributor.author | Xia, H | ||||||
|---|---|---|---|---|---|---|---|
| dc.contributor.author | Ng, SS | ||||||
| dc.contributor.author | Jiang, S | ||||||
| dc.contributor.author | Cheung, WKC | ||||||
| dc.contributor.author | Sze, J | ||||||
| dc.contributor.author | Bian, XW | ||||||
| dc.contributor.author | Kung, Hf | ||||||
| dc.contributor.author | Lin, MC | ||||||
| dc.date.accessioned | 2010-09-06T06:14:12Z | ||||||
| dc.date.available | 2010-09-06T06:14:12Z | ||||||
| dc.date.issued | 2010 | ||||||
| dc.description.abstract | Nasopharyngeal carcinoma (NPC), a highly metastatic and invasive malignant tumor originating from the nasopharynx, is widely prevalent in Southeast Asia, the Middle East and North Africa. Although viral, dietary and genetic factors have been implicated in NPC, the molecular basis of its pathogenesis is not well defined. Based on a recent microRNA (miRNA) microarray study showing miR-200 downregulation in NPC, we further investigated the role of miR-200a in NPC carcinogenesis. We found that the endogenous miR-200a expression level increases with the degree of differentiation in a panel of NPC cell lines, namely undifferentiated C666-1, high-differentiated CNE-1, and low-differentiated CNE-2 and HNE1 cells. By a series of gain-of-function and loss-of-function studies, we showed that over-expression of miR-200a inhibits C666-1 cell growth, migration and invasion, whereas its knock-down stimulates these processes in CNE-1 cells. In addition, we further identified ZEB2 and CTNNB1 as the functional downstream targets of miR-200a. Interestingly, knock-down of ZEB2 solely impeded NPC cell migration and invasion, whereas CTNNB1 suppression only inhibited NPC cell growth, suggesting that the inhibitory effects of miR-200a on NPC cell growth, migration and invasion are mediated by distinct targets and pathways. Our results reveal the important role of miR-200a as a regulatory factor of NPC carcinogenesis and a potential candidate for miRNA-based therapy against NPC. © 2009 Elsevier Inc. All rights reserved. | ||||||
| dc.description.nature | Link_to_subscribed_fulltext | ||||||
| dc.identifier.citation | Biochemical And Biophysical Research Communications, 2010, v. 391 n. 1, p. 535-541 [How to Cite?] DOI: http://dx.doi.org/10.1016/j.bbrc.2009.11.093 | ||||||
| dc.identifier.citeulike | 6197962 | ||||||
| dc.identifier.doi | http://dx.doi.org/10.1016/j.bbrc.2009.11.093 | ||||||
| dc.identifier.epage | 541 | ||||||
| dc.identifier.hkuros | 168153 | ||||||
| dc.identifier.isi | WOS:000273624500094
Funding Information: We thank Mr. Wesley Tucker for critical reading of the paper. This work was Supported by the Research Grants Council of the Hong Kong Special Administrative Region, China (No. 467109). National Basic Research Program of China (973 Program) (Nos. 2010CB529400; 2010CB912800). | ||||||
| dc.identifier.issn | 0006-291X 2011 Impact Factor: 2.484 2011 SCImago Journal Rankings: 0.287 | ||||||
| dc.identifier.issue | 1 | ||||||
| dc.identifier.openurl | | ||||||
| dc.identifier.pmid | 19931509 | ||||||
| dc.identifier.scopus | eid_2-s2.0-72949119530 | ||||||
| dc.identifier.spage | 535 | ||||||
| dc.identifier.uri | http://hdl.handle.net/10722/69496 | ||||||
| dc.identifier.volume | 391 | ||||||
| dc.language | eng | ||||||
| dc.publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description | ||||||
| dc.publisher.place | United States | ||||||
| dc.relation.ispartof | Biochemical and Biophysical Research Communications | ||||||
| dc.relation.references | References in Scopus | ||||||
| dc.subject | β-catenin | ||||||
| dc.subject | Invasion | ||||||
| dc.subject | microRNA | ||||||
| dc.subject | Migration | ||||||
| dc.subject | Nasopharyngeal carcinoma | ||||||
| dc.title | miR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion | ||||||
| dc.type | Article |
Author Affiliations
- Li Ka Shing Institute of Health Sciences
- Institute of Molecular Technology for Drug Discovery and Synthesis, Hong Kong
- Sun Yat-Sen University
- Southwestern Hospital Chongqing