Mammary gland involution is delayed by activated Akt in transgenic mice
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Activation of the antiapoptotic protein kinase Akt is induced by a number of growth factors that regulate mammary gland development. Akt is expressed during mammary gland development, and expression decreases at the onset of involution. To address Akt actions in mammary gland development, transgenic mice were generated expressing constitutively active Akt in the mammary gland under the control of the mouse mammary tumor virus (MMTV) promoter. Analysis of mammary glands from these mice reveals a delay in both involution and the onset of apoptosis. Expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), an inhibitor of matrix metalloproteinases (MMPs), is prolonged and increased in the transgenic mice, suggesting that disruption of the MMP:TIMP ratio may contribute to the delayed mammary gland involution observed in the transgenic mice.
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The results that SCRIB mislocalization enhances Akt signaling and causes mammary morphogenesis defects are consistent with a mouse model of Akt pathway activation.
“Our results showing that SCRIB mislocalization enhances Akt signaling and results in mammary morphogenesis defects are consistent with a mouse model of Akt pathway activation (43).”
From Mislocalization of the Cell Polarity Protein Scribble Promotes Mammary Tumorigenesis and Is Associated with Basal Breast Cancer (2014) · cites this paper as [43]
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References 66 · Cited by 169
Research works printed but not linked: 1
- Richert M, Wood T 1998 Expression and regulation of insulin-like growth factors and their binding proteins in the normal breast. In: Manni A (ed) Contemporary Endocrinology: Endocrinology of Breast Cancer. Hu- mana Press, Totowa, NJ, pp 39-52
- Authors
- Schwertfeger, K. L., Richert, M. M., & Anderson, S. M.
- Affiliations
- Program in Molecular Biology (K.L.S., S.M.A.) Colorado 80262
- University of Colorado Health (US)
- Corresponding author
- Anderson, Steven M.
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2001-06-01
- Volume
- 15
- Issue
- 6
- Pages
- 867-881
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- OpenAlex
- W1968837506
- Cited by
- 169
- References
- 66
- Citations by year
- 2024: 3 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 7 · 2016: 7 · 2015: 7 · 2014: 9 · 2013: 6 · 2012: 4
- FWCI
- 7.30
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (7r01dk048845-07)
- Cancer Center, University of Colorado
- National Cancer Institute (R01CA085736, CA085736, CA-46934, P30CA046934)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-48845, R01DK053858, DK-53858)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Keywords
- mammary gland involution, Akt, constitutively active Akt, transgenic mice, apoptosis, TIMP-1, matrix metalloproteinases, MMP/TIMP ratio, mammary gland development, anti-apoptotic signaling
- MeSH terms
- Animals, Caseins, DNA-Binding Proteins, Female, Lactation, Mammary Glands, Animal, Mammary Tumor Virus, Mouse, Mice, Transgenic, Microscopy, Fluorescence, Milk Proteins, Phosphorylation, Proto-Oncogene Proteins, Immunoblotting, Trans-Activators, Apoptosis, Protein Serine-Threonine Kinases, Matrix Metalloproteinase 3, Tissue Inhibitor of Metalloproteinase-1, STAT3 Transcription Factor, STAT5 Transcription Factor, Proto-Oncogene Proteins c-akt, Mice
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