NDLI: SIRT1 is essential for oncogenic signaling by estrogen/estrogen receptor α in breast cancer

Content Provider	PubMed Central
Author	Elangovan, Selvakumar Ramachandran, Sabarish Venkatesan, Narayanan Ananth, Sudha Gnana-prakasam, Jaya P. Martin, Pamela M. Browning, Darren D. Schoenlein, Patricia V. Prasad, Puttur D. Ganapathy, Vadivel Thangaraju, Muthusamy
Abstract	The NAD-dependent histone deacetylase SIRT1 is overexpressed and catalytically activated in a number of human cancers, but recent studies argue have actually suggested that it may function as a tumor suppressor and metastasis inhibitor in vivo. In breast cancer, SIRT1 stabilization has been suggested to contribute to the oncogenic potential of the estrogen receptor α (ERα), but SIRT1 activity has also been associated with ERα deacetylation and inactivation. In this study, we show that SIRT1 is critical for estrogen to promote breast cancer. ERα physically interacted and functionally cooperated with SIRT1 in breast cancer cells. ERα also bound to the promoter for SIRT1 and increased its transcription. SIRT1 expression induced by ERα was sufficient to activate anti-oxidant and pro-survival genes in breast cancer cells, such as catalase and glutathione peroxidase, and to inactivate tumor suppressor genes such as cyclin G2 (CCNG2) and p53. Moreover, SIRT1 inactivation eliminated estrogen/ERα-induced cell growth and tumor development, triggering apoptosis. Taken together, these results indicated that SIRT1 is required for estrogen-induced breast cancer growth. Our findings imply that the combination of SIRT1 inhibitors and anti-estrogen compounds may offer more effective treatment strategies for breast cancer.
Related Links	http://dx.doi.org/10.1158/0008-5472.can-11-1446
Ending Page	6664
Page Count	11
Starting Page	6654
File Format	PDF
ISSN	00085472
e-ISSN	15387445
Journal	Cancer research
Issue Number	21
Volume Number	71
Language	English
Publisher Date	2011-11-01
Access Restriction	Open
Subject Keyword	Cancer Research Oncology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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