ArticleMolecular cancer research : MCR2012
Differential tumorigenic potential and matriptase activation between PDGF B versus PDGF D in prostate cancer.
Article in Molecular cancer research : MCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Prostate cancer microenvironment: multidimensional regulation of immune cells, vascular system, stromal cells, and microbiota.Molecular cancer · 2024Review
- The production of recombinant platelet-derived growth factor D using the second generation modified vaccinia Ankara viral system.Protein science : a publication of the Protein Society · 2022Article
- Article
- Matriptase-Induced Phosphorylation of MET is Significantly Associated with Poor Prognosis in Invasive Bladder Cancer; an Immunohistochemical Analysis.International journal of molecular sciences · 2018Article
- Detecting Novel Urine Biomarkers for the Early Diagnosis of Prostate Cancer: Platelet Derived Growth Factor-BB as a Possible New Target.Current urology · 2018Article
- Article
- Identification of zinc finger protein of the cerebellum 5 as a survival factor of prostate and colorectal cancer cells.Cancer science · 2017Article
- PDGFs and their receptors.Gene · 2017Review
- PDGF-D promotes cell growth, aggressiveness, angiogenesis and EMT transformation of colorectal cancer by activation of Notch1/Twist1 pathway.Oncotarget · 2017Article
- Antiproliferation effect of imatinib mesylate on MCF7, T-47D tumorigenic and MCF 10A nontumorigenic breast cell lines via PDGFR-β, PDGF-BB, c-Kit and SCF genes.Drug design, development and therapy · 2017Article
- Article
- Bone Metastasis from Renal Cell Carcinoma.International journal of molecular sciences · 2016Review
- The interaction between androgen receptor and PDGF-D in the radiation response of prostate carcinoma.The Prostate · 2016Article
- Matriptase activation and shedding through PDGF-D-mediated extracellular acidosis.American journal of physiology. Cell physiology · 2016Article
- Dynamic regulation of platelet-derived growth factor D (PDGF-D) activity and extracellular spatial distribution by matriptase-mediated proteolysis.The Journal of biological chemistry · 2015Article
- Matriptase and MET are prominently expressed at the site of bone metastasis in renal cell carcinoma: immunohistochemical analysis.Human cell · 2015Article
- Identifying New Candidate Genes and Chemicals Related to Prostate Cancer Using a Hybrid Network and Shortest Path Approach.Computational and mathematical methods in medicine · 2015Article
- A critical role of the PTEN/PDGF signaling network for the regulation of radiosensitivity in adenocarcinoma of the prostate.International journal of radiation oncology, biology, physics · 2014Article
- Targeting the PDGF signaling pathway in tumor treatment.Cell communication and signaling : CCS · 2013Review
- Emerging roles of PDGF-D in EMT progression during tumorigenesis.Cancer treatment reviews · 2013Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The platelet-derived growth factors (PDGF A, B, C, and D) and their receptors (α-PDGFR and β-PDGFR) play an indispensible role in physiologic and pathologic conditions, including tumorigenesis. The transformative β-PDGFR is overexpressed and activated during prostate cancer progression, but the identification and functional significance of its complementary ligand have not been elucidated. This study examined potential oncogenic functions of β-PDGFR ligands PDGF B and PDGF D, using nonmalignant prostate epithelial cells engineered to overexpress these ligands. In our models, PDGF D induced cell migration and invasion more effectively than PDGF B in vitro. Importantly, PDGF D supported prostate epithelial cell tumorigenesis in vivo and showed increased tumor angiogenesis compared with PDGF B. Autocrine signaling analysis of the mitogen-activated protein kinase and phosphoinositide 3-kinase pathways found PDGF D-specific activation of the c-jun-NH2-kinase (JNK) signaling cascade. Using short hairpin RNA and pharmacologic inhibitors, we showed that PDGFD-mediated phenotypic transformation is β-PDGFR and JNK dependent. Importantly, we made a novel finding of PDGF D-specific increase in the shedding and activation of the serine protease matriptase in prostate epithelial cells. Our study, for the first time to our knowledge, showed ligand-specific β-PDGFR signaling as well as PDGF D-specific regulation of matriptase activity and its spatial distribution through shedding. Taken together with our previous finding that matriptase is a proteolytic activator of PDGF D, this study provides a molecular insight into signal amplification of the proteolytic network and PDGF signaling loop during cancer progression.
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Registered trials
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