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DNMT3B Overexpression by Deregulation of FOXO3a-Mediated Transcription Repression and MDM2 Overexpression in Lung Cancer

DNMT3B Overexpression by Deregulation of FOXO3a-Mediated Transcription Repression and MDM2... ORIGINAL ARTICLE DNMT3B Overexpression by Deregulation of FOXO3a- Mediated Transcription Repression and MDM2  Overexpression in Lung Cancer Yi-Chieh Yang, MS,* Yen-An Tang, PhD,† Jiunn-Min Shieh, MD,‡ Ruo-Kai Lin, PhD,§ Han-Shui Hsu, MD, PhD,‖ and Yi-Ching Wang, PhD*† correlated with poor prognosis examined by immunohistochemistry Introduction: DNA methyltransferase 3B (DNMT3B) contributes to and Kaplan-Meier survival analysis. de novo DNA methylation and its overexpression promotes tumori- Conclusions: We reveal a new mechanism that FOXO3a transcrip- genesis. However, whether DNMT3B is upregulated by transcrip- tionally represses DNMT3B expression and this regulation can be tional deregulation remains unclear. attenuated by MDM2 overexpression in human lung cancer model. Methods: We studied the transcriptional repression of DNMT3B by Cotreatment with doxorubicin and Nutlin-3 is a novel therapeutic forkhead O transcription factor 3a (FOXO3a) in lung cancer cell, strategy through epigenetic modulation. animal, and clinical models. Key Words: DNMT3B, FOXO3a, MDM2, Doxorubicin, Nutlin-3, Results: The results of luciferase reporter assay showed that FOXO3a Prognosis, Lung cancer negatively regulated DNMT3B promoter activity by preferentially interacting with the binding element FOXO3a-E (+166 to +173) of (J Thorac Oncol. 2014;9: 1305–1315) DNMT3B promoter. Ectopically overexpressed FOXO3a or com- bined treatment with doxorubicin to induce FOXO3a nuclear accu- mulation further bound at the distal site, FOXO3a-P (−249 to −242) n the past http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Thoracic Oncology Wolters Kluwer Health

DNMT3B Overexpression by Deregulation of FOXO3a-Mediated Transcription Repression and MDM2 Overexpression in Lung Cancer

Wang, Yi-Ching
Journal of Thoracic Oncology , Volume 9 (9) – Sep 1, 2014
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Copyright
Copyright © 2014 by the International Association for the Study of Lung Cancer
ISSN
1556-0864
DOI
10.1097/JTO.0000000000000240
pmid
25122426
Publisher site
See Article on Publisher Site

Abstract

ORIGINAL ARTICLE DNMT3B Overexpression by Deregulation of FOXO3a- Mediated Transcription Repression and MDM2  Overexpression in Lung Cancer Yi-Chieh Yang, MS,* Yen-An Tang, PhD,† Jiunn-Min Shieh, MD,‡ Ruo-Kai Lin, PhD,§ Han-Shui Hsu, MD, PhD,‖ and Yi-Ching Wang, PhD*† correlated with poor prognosis examined by immunohistochemistry Introduction: DNA methyltransferase 3B (DNMT3B) contributes to and Kaplan-Meier survival analysis. de novo DNA methylation and its overexpression promotes tumori- Conclusions: We reveal a new mechanism that FOXO3a transcrip- genesis. However, whether DNMT3B is upregulated by transcrip- tionally represses DNMT3B expression and this regulation can be tional deregulation remains unclear. attenuated by MDM2 overexpression in human lung cancer model. Methods: We studied the transcriptional repression of DNMT3B by Cotreatment with doxorubicin and Nutlin-3 is a novel therapeutic forkhead O transcription factor 3a (FOXO3a) in lung cancer cell, strategy through epigenetic modulation. animal, and clinical models. Key Words: DNMT3B, FOXO3a, MDM2, Doxorubicin, Nutlin-3, Results: The results of luciferase reporter assay showed that FOXO3a Prognosis, Lung cancer negatively regulated DNMT3B promoter activity by preferentially interacting with the binding element FOXO3a-E (+166 to +173) of (J Thorac Oncol. 2014;9: 1305–1315) DNMT3B promoter. Ectopically overexpressed FOXO3a or com- bined treatment with doxorubicin to induce FOXO3a nuclear accu- mulation further bound at the distal site, FOXO3a-P (−249 to −242) n the past

Journal

Journal of Thoracic Oncology – Wolters Kluwer Health

Published: Sep 1, 2014

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