ArticleProceedings of the National Academy of Sciences of the United States of America2012
Sprouty genes function in suppression of prostate tumorigenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Multiple endocrine defects in adult-onset Sprouty1/2/4 triple knockout mice.Scientific reports · 2024Article
- Sprouty1 is a broad mediator of cellular senescence.Cell death & disease · 2024Article
- TRAF7-targeted HOXA5 acts as a tumor suppressor in prostate cancer progression and stemness via transcriptionally activating SPRY2 and regulating MEK/ERK signaling.Cell death discovery · 2023Article
- Loss of SPRY2 contributes to cancer-associated fibroblasts activation and promotes breast cancer development.Breast cancer research : BCR · 2023Article
- The olfactory receptor OR51E2 activates ERK1/2 through the Golgi-localized Gβγ-PI3Kγ-ARF1 pathway in prostate cancer cells.Frontiers in pharmacology · 2022Article
- Mechanistic insights explain the transforming potential of the T507K substitution in the protein-tyrosine phosphatase SHP2.The Journal of biological chemistry · 2020Article
- Article
- miR-21 promotes EGF-induced pancreatic cancer cell proliferation by targeting Spry2.Cell death & disease · 2018Article
- Sprouty2 loss-induced IL6 drives castration-resistant prostate cancer through scavenger receptor B1.EMBO molecular medicine · 2018Article
- Sprouty2 inhibits amphiregulin-induced down-regulation of E-cadherin and cell invasion in human ovarian cancer cells.Oncotarget · 2016Article
- The role of wild type RAS isoforms in cancer.Seminars in cell & developmental biology · 2016Review
- Article
- KRAS(G12D)-mediated oncogenic transformation of thyroid follicular cells requires long-term TSH stimulation and is regulated by SPRY1.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Deregulation of the Ras-Erk Signaling Axis Modulates the Enhancer Landscape.Cell reports · 2015Article
- Erk Negative Feedback Control Enables Pre-B Cell Transformation and Represents a Therapeutic Target in Acute Lymphoblastic Leukemia.Cancer cell · 2015Article
- Androgen-regulation of the protein tyrosine phosphatase PTPRR activates ERK1/2 signalling in prostate cancer cells.BMC cancer · 2015Article
- Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer: a working hypothesis.BioMed research international · 2015Article
- The developing story of Sprouty and cancer.Cancer metastasis reviews · 2014Review
- Sprouty1 induces a senescence-associated secretory phenotype by regulating NFκB activity: implications for tumorigenesis.Cell death and differentiation · 2014Article
- PI3K regulates branch initiation and extension of cultured mammary epithelia via Akt and Rac1 respectively.Developmental biology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Expression of Sprouty genes is frequently decreased or absent in human prostate cancer, implicating them as suppressors of tumorigenesis. Here we show they function in prostate tumor suppression in the mouse. Concomitant inactivation of Spry1 and Spry2 in prostate epithelium causes ductal hyperplasia and low-grade prostatic intraepithelial neoplasia (PIN). However, when Spry1 and Spry2 loss-of-function occurs in the context of heterozygosity for a null allele of the tumor suppressor gene Pten, there is a striking increase in PIN and evidence of neoplastic invasion. Conversely, expression of a Spry2 gain-of-function transgene in Pten null prostatic epithelium suppresses the tumorigenic effects of loss of Pten function. We show that Sprouty gene loss-of-function results in hyperactive RAS/ERK1/2 signaling throughout the prostate epithelium and cooperates with heterozygosity for a Pten null allele to promote hyperactive PI3K/AKT signaling. Furthermore, Spry2 gain-of-function can suppress hyperactivation of AKT caused by the absence of PTEN. Together, these results point to a key genetic interaction between Sprouty genes and Pten in prostate tumorigenesis and provide strong evidence that Sprouty genes can function to modulate signaling via the RAS/ERK1/2 and PI3K/AKT pathways. The finding that Sprouty genes suppress tumorigenesis caused by Pten loss-of-function suggests that therapeutic approaches aimed at restoring normal feedback mechanisms triggered by receptor tyrosine kinase signaling, including Sprouty gene expression, may provide an effective strategy to delay or prevent high-grade PIN and invasive prostate cancer.
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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.