NDLI: Conditional overexpression of active transforming growth factor beta1 in vivo accelerates metastases of transgenic mammary tumors.

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Conditional overexpression of active transforming growth factor beta1 in vivo accelerates metastases of transgenic mammary tumors.

Content Provider	Semantic Scholar
Author	Muraoka-Cook, Rebecca S. Kurokawa, Hirokazu Koh, Yasuhiro Forbes, James T. Roebuck, L. Renee Barcellos-Hoff, Mary Helen Moody, Susan E. Chodosh, Lewis A. Arteaga, Carlos L.
Copyright Year	2004
Abstract	To address the role of transforming growth factor (TGF) beta in the progression of established tumors while avoiding the confounding inhibitory effects of TGF-beta on early transformation, we generated doxycycline (DOX)-inducible triple transgenic mice in which active TGF-beta1 expression could be conditionally regulated in mouse mammary tumor cells transformed by the polyomavirus middle T antigen. DOX-mediated induction of TGF-beta1 for as little as 2 weeks increased lung metastases >10-fold without a detectable effect on primary tumor cell proliferation or tumor size. DOX-induced active TGF-beta1 protein and nuclear Smad2 were restricted to cancer cells, suggesting a causal association between autocrine TGF-beta and increased metastases. Antisense-mediated inhibition of TGF-beta1 in polyomavirus middle T antigen-expressing tumor cells also reduced basal cell motility, survival, anchorage-independent growth, tumorigenicity, and metastases. Therefore, induction and/or activation of TGF-beta in hosts with established TGF-beta-responsive cancers can rapidly accelerate metastatic progression.
File Format	PDF HTM / HTML
DOI	10.1158/0008-5472.CAN-04-2111
PubMed reference number	15604265
Journal	Medline
Volume Number	64
Issue Number	24
Alternate Webpage(s)	http://cancerres.aacrjournals.org/content/canres/64/24/9002.full.pdf
Alternate Webpage(s)	https://doi.org/10.1158/0008-5472.CAN-04-2111
Journal	Cancer research
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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