ArticleCell death & disease2012
BRCA1 negatively regulates IGF-1 expression through an estrogen-responsive element-like site.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
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- The Role of Cow's Milk Consumption in Breast Cancer Initiation and Progression.Current nutrition reports · 2023Review
- miRNA deregulation and relationship with metabolic parameters after Mediterranean dietary intervention in BRCA-mutated women.Frontiers in oncology · 2023Article
- Effect of Inactivation ofJournal of the Endocrine Society · 2022Article
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- Obesity: a perfect storm for carcinogenesis.Cancer metastasis reviews · 2022Review
- GASP1 enhances malignant phenotypes of breast cancer cells and decreases their response to paclitaxel by forming a vicious cycle with IGF1/IGF1R signaling pathway.Cell death & disease · 2022Article
- Review
- Energy homeostasis genes modify the association between serum concentrations of IGF-1 and IGFBP-3 and breast cancer risk.Scientific reports · 2022Article
- BRCA1 Antibodies Matter.International journal of biological sciences · 2021Article
- The -44 C/G (rs1800972) polymorphism of the β-defensin 1 is associated with increased risk of developing type 2 diabetes mellitus.Molecular genetics & genomic medicine · 2019Article
- Elucidating the novel BRCA1 function as a non-genomic metabolic restraint in ER-positive breast cancer cell lines.Oncotarget · 2018Article
- IGF-1-induced MMP-11 expression promotes the proliferation and invasion of gastric cancer cells through the JAK1/STAT3 signaling pathway.Oncology letters · 2018Article
- Pharmacophore modeling for identification of anti-IGF-1R drugs and in-vitro validation of fulvestrant as a potential inhibitor.PloS one · 2018Article
- Disruption of STAT3-DNMT1 interaction by SH-I-14 induces re-expression of tumor suppressor genes and inhibits growth of triple-negative breast tumor.Oncotarget · 2017Article
- Ovarian transcriptome associated with reproductive senescence in the long-living Ames dwarf mice.Molecular and cellular endocrinology · 2017Article
- On metabolic reprogramming and tumor biology: A comprehensive survey of metabolism in breast cancer.Oncotarget · 2016Review
- A high-throughput AO/PI-based cell concentration and viability detection method using the Celigo image cytometry.Cytotechnology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The insulin-like growth factor-1 receptor (IGF-1R) signaling pathway is critical for both normal mammary gland development and malignant transformation. It has been reported that the IGF-1 stimulates breast cancer cell proliferation and is upregulated in tumors with BRCA1/2 mutations. We report here that IGF-1 is negatively regulated by BRCA1 at the transcriptional level in human breast cancer cells. BRCA1 knockdown (BRCA1-KD) induces the expression of IGF-1 mRNA in MCF7 cells in an estrogen receptor α (ERα)-dependent manner. We found that both BRCA1 and ERα bind to the endogenous IGF-1 promoter region containing an estrogen-responsive element-like (EREL) site. BRCA1-KD does not significantly affect ERα binding on the IGF-1 promoter. Reporter analysis demonstrates that BRCA1 could regulate IGF-1 transcripts via this EREL site. In addition, enzyme-linked immunosorbent assay revealed that de-repression of IGF-1 transcription by BRCA1-KD increases the level of extracellular IGF-1 protein, and secreted IGF-1 seems to increase the phospho-IGF-1Rβ and activate its downstream signaling pathway. Blocking the IGF-1/IGF-1R/phosphoinositide 3-kinase (PI3K)/AKT pathway either by a neutralizing antibody or by small-molecule inhibitors preferentially reduces the proliferation of BRCA1-KD cells. Furthermore, the IGF-1-EREL-Luc reporter assay demonstrates that various inhibitors, which can inhibit the IGF-1R pathway, can suppress this reporter activity. These findings suggest that BRCA1 defectiveness keeps turning on IGF-1/PI3K/AKT signaling, which significantly contributes to increase cell survival and proliferation.
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