File Download
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1158/1538-7445.AM2012-LB-385
- WOS: WOS:000209701501242
- Find via
Supplementary
-
Citations:
- Web of Science: 0
- Appears in Collections:
Conference Paper: The role of tumor suppressing microRNA let-7 in undifferentiated nasopharyngeal carcinoma
Title | The role of tumor suppressing microRNA let-7 in undifferentiated nasopharyngeal carcinoma |
---|---|
Authors | |
Keywords | Medical sciences Oncology |
Issue Date | 2012 |
Publisher | American Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/ |
Citation | The 103rd Annual Meeting of the America Association for Cancer Research (AACR 2012), Chicago, IL., 31 March-4 April 2012. In Cancer Research, 2012, v. 72 n. 8 suppl. 1, abstract no. LB-385 How to Cite? |
Abstract | AIMS:This study aimed at evaluating the potential anti-proliferative effects of the microRNA let-7 family in nasopharyngeal carcinoma (NPC) cells. In addition, the association between let-7 suppression and DNA hypermethylation is examined. MATERIALS AND METHODS:Levels of mature let-7 family members (-a, -b, -d, -e, -g, and -i) in normal nasopharyngeal cells (NP69 and NP460) and nasopharyngeal carcinoma cells (HK1 and HONE1) were measured by real-time quantitative PCR. Cell-proliferation assay and c-Myc immunohistochemical staining were performed on NPC cells transfected with let-7 precursor molecules. In addition, expression changes in let-7 family members in response to demethylating agents (5-azacytidine and zebularine) were also examined. RESULTS:In comparison with the normal nasopharyngeal cells, let-7 (-a, -b, -d, -e, -g, and -i) levels were reduced in nasopharyngeal carcinoma cells. Ectopic expression of the let-7 family in nasopharyngeal carcinoma cells resulted in inhibition of cell proliferation through downregulation of c-Myc expression. Demethylation treatment of nasopharyngeal carcinoma cells caused activation of let-7 expression in poorly differentiated nasopharyngeal carcinoma cells only. CONCLUSION:Our results suggested that miRNA let-7 might play a role in the proliferation of NPC. DNA methylation is a potential regulatory pathway, which is affected when let-7 is suppressed in NPC cells. However, the extent of DNA hypermethylation/hypomethylation in regulating let-7 expression requires further elucidation. |
Description | Conference Theme: Accelerating Science: Concept to Clinic Poster Session 37: Late-Breaking Poster Presentations - Epigenetics: abstract no. LB-385 This journal suppl. entitled: Proceedings: AACR 103rd Annual Meeting ... 2012 |
Persistent Identifier | http://hdl.handle.net/10722/194797 |
ISSN | 2023 Impact Factor: 12.5 2023 SCImago Journal Rankings: 3.468 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wong, TS | en_US |
dc.contributor.author | Gao, W | en_US |
dc.contributor.author | Li, JZH | en_US |
dc.contributor.author | Chan, JYW | - |
dc.date.accessioned | 2014-02-17T02:10:25Z | - |
dc.date.available | 2014-02-17T02:10:25Z | - |
dc.date.issued | 2012 | en_US |
dc.identifier.citation | The 103rd Annual Meeting of the America Association for Cancer Research (AACR 2012), Chicago, IL., 31 March-4 April 2012. In Cancer Research, 2012, v. 72 n. 8 suppl. 1, abstract no. LB-385 | en_US |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.uri | http://hdl.handle.net/10722/194797 | - |
dc.description | Conference Theme: Accelerating Science: Concept to Clinic | - |
dc.description | Poster Session 37: Late-Breaking Poster Presentations - Epigenetics: abstract no. LB-385 | - |
dc.description | This journal suppl. entitled: Proceedings: AACR 103rd Annual Meeting ... 2012 | - |
dc.description.abstract | AIMS:This study aimed at evaluating the potential anti-proliferative effects of the microRNA let-7 family in nasopharyngeal carcinoma (NPC) cells. In addition, the association between let-7 suppression and DNA hypermethylation is examined. MATERIALS AND METHODS:Levels of mature let-7 family members (-a, -b, -d, -e, -g, and -i) in normal nasopharyngeal cells (NP69 and NP460) and nasopharyngeal carcinoma cells (HK1 and HONE1) were measured by real-time quantitative PCR. Cell-proliferation assay and c-Myc immunohistochemical staining were performed on NPC cells transfected with let-7 precursor molecules. In addition, expression changes in let-7 family members in response to demethylating agents (5-azacytidine and zebularine) were also examined. RESULTS:In comparison with the normal nasopharyngeal cells, let-7 (-a, -b, -d, -e, -g, and -i) levels were reduced in nasopharyngeal carcinoma cells. Ectopic expression of the let-7 family in nasopharyngeal carcinoma cells resulted in inhibition of cell proliferation through downregulation of c-Myc expression. Demethylation treatment of nasopharyngeal carcinoma cells caused activation of let-7 expression in poorly differentiated nasopharyngeal carcinoma cells only. CONCLUSION:Our results suggested that miRNA let-7 might play a role in the proliferation of NPC. DNA methylation is a potential regulatory pathway, which is affected when let-7 is suppressed in NPC cells. However, the extent of DNA hypermethylation/hypomethylation in regulating let-7 expression requires further elucidation. | - |
dc.language | eng | en_US |
dc.publisher | American Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/ | - |
dc.relation.ispartof | Cancer Research | en_US |
dc.subject | Medical sciences | - |
dc.subject | Oncology | - |
dc.title | The role of tumor suppressing microRNA let-7 in undifferentiated nasopharyngeal carcinoma | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Wong, TS: wongtsa@hkucc.hku.hk | en_US |
dc.identifier.email | Gao, W: weigaoi@hku.hk | en_US |
dc.identifier.email | Chan, JYW: jywchan1@hku.hk | en_US |
dc.identifier.authority | Wong, TS=rp00478 | en_US |
dc.identifier.authority | Chan, JYW=rp01314 | en_US |
dc.description.nature | postprint | - |
dc.identifier.doi | 10.1158/1538-7445.AM2012-LB-385 | - |
dc.identifier.hkuros | 227804 | en_US |
dc.identifier.volume | 72 | - |
dc.identifier.issue | 8 suppl. 1 | - |
dc.identifier.isi | WOS:000209701501242 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0008-5472 | - |