ArticleThe Journal of biological chemistry2010
Prolactin enhances insulin-like growth factor I receptor phosphorylation by decreasing its association with the tyrosine phosphatase SHP-2 in MCF-7 breast cancer cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Trial
- Milk Exosomal microRNAs: Postnatal Promoters of β Cell Proliferation but Potential Inducers of β Cell De-Differentiation in Adult Life.International journal of molecular sciences · 2022Review
- Overexpression of cytoplasmic dynamin 2 is associated with worse outcomes in patients with clear cell renal cell carcinoma.Cancer biomarkers : section A of Disease markers · 2022Article
- Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022Review
- A review of Dynamin 2 involvement in cancers highlights a promising therapeutic target.Journal of experimental & clinical cancer research : CR · 2021Review
- Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.PloS one · 2021Article
- Inhibition of the Activity of Cyclophilin A Impedes Prolactin Receptor-Mediated Signaling, Mammary Tumorigenesis, and Metastases.iScience · 2020Article
- Prolactin activates ERα in the absence of ligand in female mammary development and carcinogenesis in vivo.Endocrinology · 2013Article
- IGF-1R modulation of acute GH-induced STAT5 signaling: role of protein tyrosine phosphatase activity.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Src kinases in chondrosarcoma chemoresistance and migration: dasatinib sensitises to doxorubicin in TP53 mutant cells.British journal of cancer · 2013Article
- Leptin's role in lipodystrophic and nonlipodystrophic insulin-resistant and diabetic individuals.Endocrine reviews · 2013Review
- IGF-I signaling is essential for FSH stimulation of AKT and steroidogenic genes in granulosa cells.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Article
- Prolactin receptor is a negative prognostic factor in patients with squamous cell carcinoma of the head and neck.British journal of cancer · 2011Article
- Synergy in ERK activation by cytokine receptors and tyrosine kinase growth factor receptors.Cellular signalling · 2011Article
- Unexploited therapies in breast and prostate cancer: blockade of the prolactin receptor.Trends in endocrinology and metabolism: TEM · 2010Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Normal mammary development requires coordinated interactions of numerous factors, including prolactin (PRL) and insulin-like growth factor I (IGF-I), both of which have also been implicated in breast cancer pathogenesis and progression. We previously reported that PRL and IGF-I synergize in breast cancer cells to activate ERK1/2 and AKT, leading to increased proliferation, survival, and invasion. Intriguingly, PRL co-treatment with IGF-I augments IGF-I receptor (IGF-IR) phosphorylation 2-fold higher than IGF-I alone. Here, we showed the importance of the tyrosine phosphatase SHP-2 in this cross-talk using pharmacological inhibition and small interfering RNA. SHP-2 recruitment to IGF-IR was significantly attenuated by PRL co-treatment. Src family kinase activity was required for IGF-IR association with SHP-2, ligand-induced IGF-IR internalization, and PRL-enhanced IGF-IR phosphorylation. Inhibition of internalization, via knockdown of the GTPase, dynamin-2, prevented not only IGF-IR dephosphorylation, but also PRL-enhanced IGF-IR phosphorylation. Consistently, PRL diminished IGF-I-induced IGF-IR internalization, which may result from reduced SHP-2 association with IGF-IR, because we demonstrated an essential role for SHP-2 in IGF-IR internalization. Together, these findings describe a novel mechanism of cross-talk between PRL and IGF-I in breast cancer cells, with implications for our understanding of tumor progression and potential therapeutic strategies.
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