ArticleOncotarget2015
CRIPTO overexpression promotes mesenchymal differentiation in prostate carcinoma cells through parallel regulation of AKT and FGFR activities.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting Aggressive Prostate Carcinoma Cells with Mesothelin-CAR-T Cells.Biomedicines · 2025Article
- CRIPTO's multifaceted role in driving aggressive prostate cancer unveiled by in vivo, organoid, and patient data.Oncogene · 2025Article
- Long-term zinc treatment alters the mechanical properties and metabolism of prostate cancer cells.Cancer cell international · 2024Article
- A novel intronic circular RNA circFGFR1Journal of translational medicine · 2023Article
- Article
- Whence CRIPTO: The Reemergence of an Oncofetal Factor in 'Wounds' That Fail to Heal.International journal of molecular sciences · 2021Review
- Extracellular Vesicles in Advanced Prostate Cancer: Tools to Predict and Thwart Therapeutic Resistance.Cancers · 2021Review
- Role of Hypoxic Stress in Regulating Tumor Immunogenicity, Resistance and Plasticity.International journal of molecular sciences · 2018Review
- Synergistic anti-angiogenic treatment effects by dual FGFR1 and VEGFR1 inhibition in FGFR1-amplified breast cancer.Oncogene · 2018Article
- Knockdown of Cripto-1 inhibits the proliferation, migration, invasion, and angiogenesis in prostate carcinoma cells.Journal of biosciences · 2017Article
- CRIPTO and its signaling partner GRP78 drive the metastatic phenotype in human osteotropic prostate cancer.Oncogene · 2017Article
- JARID2 promotes invasion and metastasis of hepatocellular carcinoma by facilitating epithelial-mesenchymal transition through PTEN/AKT signaling.Oncotarget · 2016Article
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Corrections and comments
- Erratum issued
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the EGF-CFC (Cripto, FRL-1, Cryptic) protein family are increasingly recognized as key mediators of cell movement and cell differentiation during vertebrate embryogenesis. The founding member of this protein family, CRIPTO, is overexpressed in various human carcinomas. Yet, the biological role of CRIPTO in this setting remains unclear. Here, we find CRIPTO expression as especially high in a subgroup of primary prostate carcinomas with poorer outcome, wherein resides cancer cell clones with mesenchymal traits. Experimental studies in PCa models showed that one notable function of CRIPTO expression in prostate carcinoma cells may be to augment PI3K/AKT and FGFR1 signaling, which promotes epithelial-mesenchymal transition and sustains a mesenchymal state. In the observed signaling events, FGFR1 appears to function parallel to AKT, and the two pathways act cooperatively to enhance migratory, invasive and transformation properties specifically in the CRIPTO overexpressing cells. Collectively, these findings suggest a novel molecular network, involving CRIPTO, AKT, and FGFR signaling, in favor of the emergence of mesenchymal-like cancer cells during the development of aggressive prostate tumors.
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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.