ArticleCell death and differentiation2012
Constitutive activation of JAK2 in mammary epithelium elevates Stat5 signalling, promotes alveologenesis and resistance to cell death, and contributes to tumourigenesis.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Activation of M1mAChR's improves spatial learning and memory deficits in rats exposed to chronic intermittent hypoxia.Scientific reports · 2026Article
- Review
- Developmental Regulation of circRNAs in Normal and Diseased Mammary Gland: A Focus on circRNA-miRNA Networks.Journal of mammary gland biology and neoplasia · 2025Review
- Mcam stabilizes a luminal progenitor-like breast cancer cell state via Ck2 control and Src/Akt/Stat3 attenuation.NPJ breast cancer · 2024Article
- JAK: Not Just Another Kinase.Molecular cancer therapeutics · 2022Review
- Germline Variants Associated with Nasopharyngeal Carcinoma Predisposition Identified through Whole-Exome Sequencing.Cancers · 2022Article
- Article
- Current Evidences and Future Perspectives for AMPK in the Regulation of Milk Production and Mammary Gland Biology.Frontiers in cell and developmental biology · 2020Review
- Cyclophilin A Function in Mammary Epithelium Impacts Jak2/Stat5 Signaling, Morphogenesis, Differentiation, and Tumorigenesis in the Mammary Gland.Cancer research · 2018Article
- STAT3 activation in infection and infection-associated cancer.Molecular and cellular endocrinology · 2017Review
- Crosstalk between STAT5 activation and PI3K/AKT functions in normal and transformed mammary epithelial cells.Molecular and cellular endocrinology · 2017Review
- The crossroads of breast cancer progression: insights into the modulation of major signaling pathways.OncoTargets and therapy · 2017Review
- Foxa1 is essential for mammary duct formation.Genesis (New York, N.Y. : 2000) · 2016Article
- C14orf166 overexpression correlates with tumor progression and poor prognosis of breast cancer.Journal of translational medicine · 2016Article
- Stat5 regulates the phosphatidylinositol 3-kinase/Akt1 pathway during mammary gland development and tumorigenesis.Molecular and cellular biology · 2014Article
- Dysregulated STAT1-SOCS1 control of JAK2 promotes mammary luminal progenitor cell survival and drives ERα(+) tumorigenesis.Cell death and differentiation · 2014Article
- Distinct roles of STAT3 and STAT5 in the pathogenesis and targeted therapy of breast cancer.Molecular and cellular endocrinology · 2014Review
- STAT signaling in mammary gland differentiation, cell survival and tumorigenesis.Molecular and cellular endocrinology · 2014Review
- Targeting the insulin growth factor and the vascular endothelial growth factor pathways in ovarian cancer.Molecular cancer therapeutics · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Signalling through the janus kinase (JAK)/signal transducer and activator of transcription (Stat) pathway is required at different stages of mammary gland development, and this pathway is frequently hyper-activated in cancer, including tumours of the breast. Stats 3, 5 and 6 have important roles in the differentiation and survival of mammary alveolar cells, but somewhat paradoxically, both Stat3 and 5 can have oncogenic activity in the mammary gland. Constitutive activation of JAK2 could be anticipated to result in hyper-activation of Stats 1, 3, 5 and 6 with concomitant cell transformation, although the outcome is difficult to envisage, particularly since Stats 3 and 5 play opposing roles in normal mammary gland development. Here, we show that expression of a constitutively active JAK2 mutant, JAK2 V617F, leads to hyper-activation of Stat5 in mammary epithelial cells (MECs), and transgenic mice expressing JAK2 V617F specifically in the mammary gland exhibit accelerated alveologenesis during pregnancy and delayed post-lactational regression. Overexpressing JAK2 V617F in MECs in vitro results in elevated proliferation and resistance to cell death. Furthermore, constitutively active JAK2 enhances anchorage-independent cell growth in the presence of a co-operating oncogene and accelerates tumourigenesis in a xenograft model. Taken together, our results provide insights into signalling downstream of constitutively active JAK2 and could be important for understanding the molecular mechanisms of breast tumourigenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.