ArticleOncogene2006
Loss of Sef (similar expression to FGF) expression is associated with high grade and metastatic prostate cancer.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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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.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Transcending frontiers in prostate cancer: the role of oncometabolites on epigenetic regulation, CSCs, and tumor microenvironment to identify new therapeutic strategies.Cell communication and signaling : CCS · 2024Review
- The role of interleukin-17 in inflammation-related cancers.Frontiers in immunology · 2024Review
- Golgi Complex: A Signaling Hub in Cancer.Cells · 2022Review
- Soluble Endoglin Stimulates Inflammatory and Angiogenic Responses in Microglia That Are Associated with Endothelial Dysfunction.International journal of molecular sciences · 2022Article
- Immunoreactivity against fibroblast growth factor 8 in alveolar rhabdomyosarcoma patients and its involvement in tumor aggressiveness.Oncoimmunology · 2022Article
- Interleukin-17 receptor D (Sef) is a multi-functional regulator of cell signaling.Cell communication and signaling : CCS · 2021Review
- Interleukin-17 Receptor D in Physiology, Inflammation and Cancer.Frontiers in oncology · 2021Review
- Loss of interleukin-17 receptor D promotes chronic inflammation-associated tumorigenesis.Oncogene · 2021Article
- Delivery of the gene encoding the tumor suppressor Sef into prostate tumors by therapeutic-ultrasound inhibits both tumor angiogenesis and growth.Scientific reports · 2017Article
- Loss of hSef promotes metastasis through upregulation of EMT in prostate cancer.International journal of cancer · 2017Article
- Sef Regulates Epithelial-Mesenchymal Transition in Breast Cancer Cells.Journal of cellular biochemistry · 2016Article
- Aberrant expression of hSef and Sprouty4 in endometrial adenocarcinoma.Oncology letters · 2016Article
- Characterization of Golgi scaffold proteins and their roles in compartmentalizing cell signaling.Journal of molecular histology · 2014Review
- Targeting fibroblast growth factor receptor signaling inhibits prostate cancer progression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- Identification of a clinically relevant androgen-dependent gene signature in prostate cancer.Cancer research · 2011Article
- Raf family kinases: old dogs have learned new tricks.Genes & cancer · 2011Article
- Sef is a negative regulator of fiber cell differentiation in the ocular lens.Differentiation; research in biological diversity · 2010Article
- Fibroblast growth factor signalling: from development to cancer.Nature reviews. Cancer · 2010Review
- Similar expression to FGF (Sef) inhibits fibroblast growth factor-induced tumourigenic behaviour in prostate cancer cells and is downregulated in aggressive clinical disease.British journal of cancer · 2009Article
- The role of fibroblast growth factors in tumor growth.Current cancer drug targets · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Fibroblast growth factors (FGF), and in particular FGF8, have been strongly implicated in prostate carcinogenesis. This study investigated the expression of Sef, a key inhibitory regulator of FGF signalling, in prostate cancer. In a panel of cell lines, hSef was detected in both androgen-dependent and independent cells but was significantly reduced in highly metastatic derivative clones. hSef expression was not influenced by androgenic stimulation. Forced downregulation of hSef by siRNA increased FGF8b induced cell migration (P=0.02) and invasion (P=0.007). Reduced hSef levels also enhanced FGF8b stimulated expression of MMP9 (P=0.005). mRNA in situ hybridization revealed hSef expression in 80% (8/10) of benign biopsies but in only 69% (23/33) of Gleason sum 4-7 and 35% (10/28) of Gleason sum 8-10 cancer biopsies (P=0.004). Quantitative PCR of microdissected glands confirmed this trend (P=0.001). hSef was expressed in 69% (27/39) of non-metastatic tumours but in only 18% (2/11) of metastatic tumours (P=0.004, n=50). hSef expression was next correlated with earlier data on FGF8b expression in a subgroup of cancers. In this cohort, 86% (19/22) of high-grade cancers expressed FGF8 but only 31% (7/22) expressed hSef. Positive FGF8 expression but a loss of hSef was observed in 88% (7/8) of metastatic tumours. In contrast, metastasis was evident in only 10% (1/10) of tumours, which co-expressed both FGF8 and hSef (P<0.001). These results suggest evidence that hSef is downregulated in advanced prostate cancer and might facilitate an enhanced tumorigenic response to FGFs. Further research into the role of hSef in cancer cell signalling and the mechanism of its downregulation may contribute to more effective targeting of growth factors in prostate cancer.
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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.