NDLI: TGFBI deficiency predisposes mice to spontaneous tumor development

Content Provider	PubMed Central
Author	Zhang, Ye Wen, Gengyun Shao, Genze Wang, Cuidong Lin, Chyuansheng Fang, Hongbo Balajee, Adayabalam S. Bhagat, Govind Hei, Tom K. Zhao, Yongliang
Abstract	Loss of TGFBI, a secreted protein induced by TGF-β, has been implicated in cell proliferation, tumor progression and angiogenesis by in vitro studies. However, in vivo anti-tumor functions of TGFBI as well as the underlying molecular mechanism are not well understood. To these aims, we have generated a mouse model with disruption of TGFBI genomic locus. Mice lacking TGFBI show a retarded growth, and are prone to spontaneous tumors and DMBA (dimethylbenz (a)anthracene)-induced skin tumors. In relative to wild type mouse embryonic fibroblasts (MEFs), TGFBI −/− MEFs display increased frequencies of chromosomal aberration and micronuclei formation, and exhibit an enhanced proliferation and early S-phase entry. Cyclin D1 is upregulated in TGFBI −/− MEFs, which correlates with aberrant activation of transcription factor CREB (cAMP-response binding protein) identified by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. TGFBI reconstitution in TGFBI −/− cells by either retroviral infection with wild type TGFBI gene or supplement with recombinant mouse TGFBI protein in the culture medium leads to the suppression of CREB activation and cyclin D1 expression, and further inhibition of cell proliferation. Cyclin D1 upregulation was also identified in most of tumors arising from TGFBI −/− mice. Our studies provide the first evidence that TGFBI functions as a tumor suppressor in vivo.
Related Links	http://dx.doi.org/10.1158/0008-5472.can-08-1648
Ending Page	44
Page Count	8
Starting Page	37
File Format	PDF
ISSN	00085472
e-ISSN	15387445
Journal	Cancer research
Issue Number	1
Volume Number	69
Language	English
Publisher Date	2009-01-01
Access Restriction	Open
Subject Keyword	Cancer Research Oncology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

Sl.	Authority	Responsibilities	Communication Details
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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9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

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