Sökning: id:"swepub:oai:gup.ub.gu.se/59602" >
Angiogenic factors ...
Angiogenic factors FGF2 and PDGF-BB synergistically promote murine tumor neovascularization and metastasis.
-
Nissen, Lars Johan (författare)
-
- Cao, Renhai (författare)
- Karolinska Institutet
-
- Hedlund, Eva-Maria (författare)
- Karolinska Institutet
-
visa fler...
-
Wang, Zongwei (författare)
-
Zhao, Xing (författare)
-
- Wetterskog, Daniel, 1978 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
-
- Funa, Keiko, 1949 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
-
Bråkenhielm, Ebba (författare)
-
- Cao, Yihai (författare)
- Karolinska Institutet
-
visa färre...
-
(creator_code:org_t)
- 2007
- 2007
- Engelska.
-
Ingår i: The Journal of clinical investigation. - 0021-9738. ; 117:10, s. 2766-77
- Relaterad länk:
-
https://gup.ub.gu.se...
-
visa fler...
-
https://doi.org/10.1...
-
http://kipublication...
-
visa färre...
Abstract
Ämnesord
Stäng
- Tumors produce multiple growth factors, but little is known about the interplay between various angiogenic factors in promoting tumor angiogenesis, growth, and metastasis. Here we show that 2 angiogenic factors frequently upregulated in tumors, PDGF-BB and FGF2, synergistically promote tumor angiogenesis and pulmonary metastasis. Simultaneous overexpression of PDGF-BB and FGF2 in murine fibrosarcomas led to the formation of high-density primitive vascular plexuses, which were poorly coated with pericytes and VSMCs. Surprisingly, overexpression of PDGF-BB alone in tumor cells resulted in dissociation of VSMCs from tumor vessels and decreased recruitment of pericytes. In the absence of FGF2, capillary ECs lacked response to PDGF-BB. However, FGF2 triggers PDGFR-alpha and -beta expression at the transcriptional level in ECs, which acquire hyperresponsiveness to PDGF-BB. Similarly, PDGF-BB-treated VSMCs become responsive to FGF2 stimulation via upregulation of FGF receptor 1 (FGFR1) promoter activity. These findings demonstrate that PDGF-BB and FGF2 reciprocally increase their EC and mural cell responses, leading to disorganized neovascularization and metastasis. Our data suggest that intervention of this non-VEGF reciprocal interaction loop for the tumor vasculature could be an important therapeutic target for the treatment of cancer and metastasis.
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
Hitta via bibliotek
Till lärosätets databas
- Av författaren/redakt...
-
Nissen, Lars Joh ...
-
Cao, Renhai
-
Hedlund, Eva-Mar ...
-
Wang, Zongwei
-
Zhao, Xing
-
Wetterskog, Dani ...
-
visa fler...
-
Funa, Keiko, 194 ...
-
Bråkenhielm, Ebb ...
-
Cao, Yihai
-
visa färre...
- Artiklar i publikationen
-
The Journal of c ...
- Av lärosätet
-
Göteborgs universitet
-
Karolinska Institutet