ArticleThe American journal of pathology2012
Role of the nuclear receptor coactivator AIB1/SRC-3 in angiogenesis and wound healing.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Role of vitamin D and calcium signaling in epidermal wound healing.Journal of endocrinological investigation · 2023Review
- Protective Prognostic Biomarkers Negatively Correlated with Macrophage M2 Infiltration in Low-Grade Glioma.Journal of oncology · 2022Article
- Wound Healing-related Functions of the p160 Steroid Receptor Coactivator Family.Endocrinology · 2021Review
- Emerging roles of steroid receptor coactivators in stromal cell responses.The Journal of endocrinology · 2021Review
- A steroid receptor coactivator stimulator (MCB-613) attenuates adverse remodeling after myocardial infarction.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Nuclear P38: Roles in Physiological and Pathological Processes and Regulation of Nuclear Translocation.International journal of molecular sciences · 2020Review
- A Review of the Contribution of Mast Cells in Wound Healing: Involved Molecular and Cellular Mechanisms.Clinical reviews in allergy & immunology · 2020Review
- Depletion of the Transcriptional Coactivator Amplified in Breast Cancer 1 (AIB1) Uncovers Functionally Distinct Subpopulations in Triple-Negative Breast Cancer.Neoplasia (New York, N.Y.) · 2019Article
- The PPARγ agonist efatutazone delays invasive progression and induces differentiation of ductal carcinoma in situ.Breast cancer research and treatment · 2018Article
- Cell growth density modulates cancer cell vascular invasion via Hippo pathway activity and CXCR2 signaling.Oncogene · 2015Article
- Article
- ERK3 promotes endothelial cell functions by upregulating SRC-3/SP1-mediated VEGFR2 expression.Journal of cellular physiology · 2014Article
- The nuclear coactivator amplified in breast cancer 1 maintains tumor-initiating cells during development of ductal carcinoma in situ.Oncogene · 2014Article
- Transcriptional repression of AIB1 by FoxG1 leads to apoptosis in breast cancer cells.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Steroid receptor coactivator-3 as a potential molecular target for cancer therapy.Expert opinion on therapeutic targets · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
The nuclear receptor coactivator amplified in breast cancer 1 (AIB1/SRC-3) has a well-defined role in steroid and growth factor signaling in cancer and normal epithelial cells. Less is known about its function in stromal cells, although AIB1/SRC-3 is up-regulated in tumor stroma and may, thus, contribute to tumor angiogenesis. Herein, we show that AIB1/SRC-3 depletion from cultured endothelial cells reduces their proliferation and motility in response to growth factors and prevents the formation of intact monolayers with tight junctions and of endothelial tubes. In AIB1/SRC-3(+/-) and (-/-) mice, the angiogenic responses to subcutaneous Matrigel implants was reduced by two-thirds, and exogenously added fibroblast growth factor (FGF) 2 did not overcome this deficiency. Furthermore, AIB1/SRC-3(+/-) and (-/-) mice showed similarly delayed healing of full-thickness excisional skin wounds, indicating that both alleles were required for proper tissue repair. Analysis of this defective wound healing showed reduced recruitment of inflammatory cells and macrophages, cytokine induction, and metalloprotease activity. Skin grafts from animals with different AIB1 genotypes and subsequent wounding of the grafts revealed that the defective healing was attributable to local factors and not to defective bone marrow responses. Indeed, wounds in AIB1(+/-) mice showed reduced expression of FGF10, FGFBP3, FGFR1, FGFR2b, and FGFR3, major local drivers of angiogenesis. We conclude that AIB1/SRC-3 modulates stromal cell responses via cross-talk with the FGF signaling pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.