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Tytuł:
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Ephrin B Activate Src Family Kinases in Fibroblasts Inducing Stromal Remodeling in Prostate Cancer.
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Autorzy:
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Kakarla M; Department of Surgery, NorthShore University HealthSystem, Research Institute, 1001 University Place, Chicago, IL 60201, USA.
ChallaSivaKanaka S; Department of Surgery, NorthShore University HealthSystem, Research Institute, 1001 University Place, Chicago, IL 60201, USA.
Dufficy MF; Department of Surgery, NorthShore University HealthSystem, Research Institute, 1001 University Place, Chicago, IL 60201, USA.
Gil V; Department of Surgery, NorthShore University HealthSystem, Research Institute, 1001 University Place, Chicago, IL 60201, USA.
Filipovich Y; Department of Surgery, NorthShore University HealthSystem, Research Institute, 1001 University Place, Chicago, IL 60201, USA.
Vickman R; Department of Surgery, NorthShore University HealthSystem, Research Institute, 1001 University Place, Chicago, IL 60201, USA.
Crawford SE; Department of Surgery, NorthShore University HealthSystem, Research Institute, 1001 University Place, Chicago, IL 60201, USA.
Hayward SW; Department of Surgery, NorthShore University HealthSystem, Research Institute, 1001 University Place, Chicago, IL 60201, USA.
Franco OE; Department of Surgery, NorthShore University HealthSystem, Research Institute, 1001 University Place, Chicago, IL 60201, USA.
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Źródło:
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Cancers [Cancers (Basel)] 2022 May 09; Vol. 14 (9). Date of Electronic Publication: 2022 May 09.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: Basel, Switzerland : MDPI
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Grant Information:
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RO1 CA24920 US National Institutes of Health/National Cancer Institute (RO1 CA24920); W81XWH-20-1-0210 Department of Defense; N/A Rob Brooks Fund for Personalized Cancer Care
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Contributed Indexing:
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Keywords: EFNB1; EFNB2; EFNB3; Ephrins; Src family kinases; Tenascin-C; carcinoma-associated fibroblasts (CAF); cytokines; paracrine signaling; prostate cancer; reverse signaling; stroma; tumor microenvironment (TME)
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Entry Date(s):
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Date Created: 20220514 Latest Revision: 20220716
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Update Code:
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20240105
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PubMed Central ID:
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PMC9102363
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DOI:
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10.3390/cancers14092336
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PMID:
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35565468
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Through stromal-epithelial interactions, carcinoma associated fibroblasts (CAF) play a critical role in tumor growth and progression. Activation of erythrophoyetin-producing human hepatocellular (Eph) receptors has been implicated in cancer. Eph receptor interactions with Ephrin ligands lead to bidirectional signals in the recipient and effector cells. The consequences of continuous reverse Ephrin signaling activation in fibroblasts on prostate cancer (PCa) is unknown. When compared to benign prostate fibroblast, CAF displayed higher expression of Ephrin B1, B2, and B3 ligands (EFNB1, EFNB2, and EFNB3). In this study, we found that continuous activation of EFNB1 and EFNB3 in a benign human prostate stromal cell line (BHPrS1) increased the expression of CAF markers and induced a CAF phenotype. BHPrS1 EFNB1 and BHPrS1 EFNB3 displayed a pro-tumorigenic secretome with multiple effects on neovascularization, collagen deposition, and cancer cell proliferation, overall increasing tumorigenicity of a premalignant prostate epithelial cell line BPH1 and PCa cell line LNCaP, both in vitro and in vivo. Inhibition of Src family kinases (SFK) in BHPrS1 EFNB1 and BHPrS1 EFNB3 suppressed EFNB-induced ɑ-SMA (Alpha-smooth muscle actin) and TN-C (Tenascin-C) in vitro. Our study suggests that acquisition of CAF characteristics via SFK activation in response to increased EFNB ligands could promote carcinogenesis via modulation of TME in PCa.
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