有哪些信誉好的足球投注网站activation of the canonical wntβ-catenin pathway in atf3-induced mammary tumors规范wntβ-catenin通路的激活atf3-induced乳腺肿瘤.pdfVIP
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activation of the canonical wntβ-catenin pathway in atf3-induced mammary tumors规范wntβ-catenin通路的激活atf3-induced乳腺肿瘤
Activation of the Canonical Wnt/b-Catenin Pathway in
ATF3-Induced Mammary Tumors
1 1 1 1 2 1
Leqin Yan , Luis Della Coletta , K. Leslie Powell , Jianjun Shen , Howard Thames , C. Marcelo Aldaz ,
Michael C. MacLeod1*
1 Department of Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, Texas, United States of America, 2 Department of
Biomathematics, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America
Abstract
Female transgenic mice that constitutively overexpress the transcription factor ATF3 in the basal epithelium of the
mammary gland develop mammary carcinomas with high frequency, but only if allowed to mate and raise pups early in life.
This transgenic mouse model system reproduces some features of human breast cancer in that about 20% of human breast
tumor specimens exhibit overexpression of ATF3 in the tumor cells. The ATF3-induced mouse tumors are phenotypically
similar to mammary tumors induced by overexpression of activating Wnt/b-catenin pathway genes. We now show that the
Wnt/b-catenin pathway is indeed activated in ATF3-induced tumors. b-catenin is transcriptionally up-regulated in the
tumors, and high levels of nuclear b-catenin are seen in tumor cells. A reporter gene for Wnt/b-catenin pathway activity,
TOPGAL, is up-regulated in the tumors and several downstream targets of Wnt signaling, including Ccnd1, Jun, Axin2 and
Dkk4, are also expressed at higher levels in ATF3-induced tumors compared to mammary glands of transgenic females.
Several positive-acting ligands for this pathway, including Wnt3, Wnt3a, Wnt7b, and Wnt5a, are significantly overexpressed
in tumor tissu
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