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Conference Paper: SIRT6 induces EMT and promotes cancer cell invasion and migration in prostate cancer

TitleSIRT6 induces EMT and promotes cancer cell invasion and migration in prostate cancer
Authors
KeywordsMedical sciences
Oncology
Issue Date2014
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
The 2014 Annual Meeting of the American Association for Cancer research (AACR 2014), San Diego, CA., 5-9 April 2014. In Cancer Research, 2014, v. 74 n. 19 suppl., abstract no. 1151 How to Cite?
AbstractProstate cancer (PCa) is the most common cancer and the second leading cause of cancer related death in males in the developed countries. One of the major clinical challenges is the propensity for advanced PCa to metastasize to bone or other organs, which is primarily responsible for its effect on patient mortality. SIRT6, one of Sirtuins family members, is an important histone modifying protein that regulates diverse physiological functions such as aging and metabolism. Recently there is much evidence showing an involvement of SIRT6 in tumorigenesis. At present, relatively little is known about the role of SIRT6 in regulating prostate cancer or metastasis. In our study, we have used both prostate tumor tissues and prostate cancer cell lines to study the roles of SIRT6 in the development and progression of PCa. From deposited gene profiling studies we found that SIRT6 was overexpressed in prostate tumors, compared with normal prostate tissues. Tissue microarray studies confirmed the higher levels of SIRT6 in both prostate tumor tissues and prostate cancer cells than in their normal counterparts. Depletion of SIRT6 by siRNA inhibited PCa cell proliferation. Bioinformatics analysis of the databases revealed that the high SIRT6 expression was associated with markedly shorter window of clinical recurrence, and the expression level of SIRT6 was significantly higher in PCa tissue with Gleason grade greater than seven. Further analysis indicated that SIRT6 expression increased along with the metastasis of PCa. We used PC-3 and DU145 cells to study whether SIRT6 could play a role in the migration and invasion of PCa cells. Indeed, SIRT6-deficiency markedly reduced cell migration and invasion. Compared with control siRNA treated cells, the protein level of N-cadherin reduced while E-cadherin level showed an increase after SIRT6 knockdown. We further revealed that SIRT6 regulated EMT-inducing transcription factor expression in PCa cells. Taken together, our findings indicate that SIRT6 is up-regulated in PCa, and the high expression of SIRT6 plays an important role in the progression of PCa as it facilitates cancer cell migration and invasion, and possibly metastasis. These data also suggest the therapeutic value of targeting SIRT6 in the treatment of metastatic PCa. ©2014 American Association for Cancer Research.
DescriptionMeeting Theme: Harnessing Breakthroughs - Targeting Cures
Session - Tumor Biology: Poster Presentations - Epithelial-Mesenchymal Transitions in Tumor Metastasis: abstract no. 1151
This journal suppl. entitled: Proceedings: AACR Annual Meeting 2014
Persistent Identifierhttp://hdl.handle.net/10722/213529
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorXie, Q-
dc.contributor.authorWong, AS-
dc.contributor.authorXia, W-
dc.date.accessioned2015-08-05T01:42:32Z-
dc.date.available2015-08-05T01:42:32Z-
dc.date.issued2014-
dc.identifier.citationThe 2014 Annual Meeting of the American Association for Cancer research (AACR 2014), San Diego, CA., 5-9 April 2014. In Cancer Research, 2014, v. 74 n. 19 suppl., abstract no. 1151-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/213529-
dc.descriptionMeeting Theme: Harnessing Breakthroughs - Targeting Cures-
dc.descriptionSession - Tumor Biology: Poster Presentations - Epithelial-Mesenchymal Transitions in Tumor Metastasis: abstract no. 1151-
dc.descriptionThis journal suppl. entitled: Proceedings: AACR Annual Meeting 2014-
dc.description.abstractProstate cancer (PCa) is the most common cancer and the second leading cause of cancer related death in males in the developed countries. One of the major clinical challenges is the propensity for advanced PCa to metastasize to bone or other organs, which is primarily responsible for its effect on patient mortality. SIRT6, one of Sirtuins family members, is an important histone modifying protein that regulates diverse physiological functions such as aging and metabolism. Recently there is much evidence showing an involvement of SIRT6 in tumorigenesis. At present, relatively little is known about the role of SIRT6 in regulating prostate cancer or metastasis. In our study, we have used both prostate tumor tissues and prostate cancer cell lines to study the roles of SIRT6 in the development and progression of PCa. From deposited gene profiling studies we found that SIRT6 was overexpressed in prostate tumors, compared with normal prostate tissues. Tissue microarray studies confirmed the higher levels of SIRT6 in both prostate tumor tissues and prostate cancer cells than in their normal counterparts. Depletion of SIRT6 by siRNA inhibited PCa cell proliferation. Bioinformatics analysis of the databases revealed that the high SIRT6 expression was associated with markedly shorter window of clinical recurrence, and the expression level of SIRT6 was significantly higher in PCa tissue with Gleason grade greater than seven. Further analysis indicated that SIRT6 expression increased along with the metastasis of PCa. We used PC-3 and DU145 cells to study whether SIRT6 could play a role in the migration and invasion of PCa cells. Indeed, SIRT6-deficiency markedly reduced cell migration and invasion. Compared with control siRNA treated cells, the protein level of N-cadherin reduced while E-cadherin level showed an increase after SIRT6 knockdown. We further revealed that SIRT6 regulated EMT-inducing transcription factor expression in PCa cells. Taken together, our findings indicate that SIRT6 is up-regulated in PCa, and the high expression of SIRT6 plays an important role in the progression of PCa as it facilitates cancer cell migration and invasion, and possibly metastasis. These data also suggest the therapeutic value of targeting SIRT6 in the treatment of metastatic PCa. ©2014 American Association for Cancer Research.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.subjectMedical sciences-
dc.subjectOncology-
dc.titleSIRT6 induces EMT and promotes cancer cell invasion and migration in prostate cancer-
dc.typeConference_Paper-
dc.identifier.emailWong, AS: awong1@hku.hk-
dc.identifier.authorityWong, AS=rp00805-
dc.identifier.doi10.1158/1538-7445.AM2014-1151-
dc.identifier.hkuros247710-
dc.identifier.volume74-
dc.identifier.issue19 suppl.-
dc.publisher.placeUnited States-

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