Role of FGF10 on tumorigenesis by MS‐K. (10th December 2013)
- Record Type:
- Journal Article
- Title:
- Role of FGF10 on tumorigenesis by MS‐K. (10th December 2013)
- Main Title:
- Role of FGF10 on tumorigenesis by MS‐K
- Authors:
- Sugimoto, Kenkichi
Yoshida, Suzuka
Mashio, Yuka
Toyota, Naoka
Xing, Yanjiang
Xu, Henan
Fujita, Yuki
Huang, Zhijun
Touma, Maki
Wu, Qiong - Abstract:
- <abstract abstract-type="main" id="gtc12118-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Murine MS‐K and NFSA cell lines formed tumor after inoculation into mouse and both cell lines expressed high level of <italic>vascular endothelial growth factor‐A</italic> (<italic>vegf‐A</italic>) and produced same level of VEGF‐A. However, poor blood vessel formation, and necrosis was significantly observed in NFSA‐tumor, contrary to well‐developed blood vessel formation in MS‐K tumor. The microarray analysis showed high expression of <italic>fibroblast growth factor‐10 (fgf‐10)</italic> in MS‐K than NFSA. In this report, the role of <italic>fgf‐10</italic> on tumor growth was studied. MS‐K enhanced more proliferation of endothelial cells by direct co‐culture than NFSA, and rFGF10 supported the proliferation of HUVEC in combination with VEGF‐A. <italic>fgf‐10‐</italic>knocked down MS‐K, MS‐K (<italic>fgf‐10</italic>‐KD), proliferated slower <italic>in vitro</italic> and the tumorigenicity of them was also slower than control. The blood vessel formation in these MS‐K (<italic>fgf‐10</italic>‐KD) clones was reduced compared with the MS‐K (normal). qPCR analysis showed the suppression of <italic>vegf‐</italic>A, <italic>vegf</italic>‐C and <italic>fgfr‐1‐expression</italic> in the MS‐K (<italic>fgf‐10</italic>‐KD) clones. Taken together, these results indicated that FGF10, which was produced from tumor cells, was essential for the proliferation of tumor cell itself<abstract abstract-type="main" id="gtc12118-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Murine MS‐K and NFSA cell lines formed tumor after inoculation into mouse and both cell lines expressed high level of <italic>vascular endothelial growth factor‐A</italic> (<italic>vegf‐A</italic>) and produced same level of VEGF‐A. However, poor blood vessel formation, and necrosis was significantly observed in NFSA‐tumor, contrary to well‐developed blood vessel formation in MS‐K tumor. The microarray analysis showed high expression of <italic>fibroblast growth factor‐10 (fgf‐10)</italic> in MS‐K than NFSA. In this report, the role of <italic>fgf‐10</italic> on tumor growth was studied. MS‐K enhanced more proliferation of endothelial cells by direct co‐culture than NFSA, and rFGF10 supported the proliferation of HUVEC in combination with VEGF‐A. <italic>fgf‐10‐</italic>knocked down MS‐K, MS‐K (<italic>fgf‐10</italic>‐KD), proliferated slower <italic>in vitro</italic> and the tumorigenicity of them was also slower than control. The blood vessel formation in these MS‐K (<italic>fgf‐10</italic>‐KD) clones was reduced compared with the MS‐K (normal). qPCR analysis showed the suppression of <italic>vegf‐</italic>A, <italic>vegf</italic>‐C and <italic>fgfr‐1‐expression</italic> in the MS‐K (<italic>fgf‐10</italic>‐KD) clones. Taken together, these results indicated that FGF10, which was produced from tumor cells, was essential for the proliferation of tumor cell itself and also supports proliferation of endothelial cells. Thus, FGF10 plays an important role for tumor growth by both paracrine and autocrine manner.</p> </abstract> … (more)
- Is Part Of:
- Genes to cells. Volume 19:Number 2(2014:Feb.)
- Journal:
- Genes to cells
- Issue:
- Volume 19:Number 2(2014:Feb.)
- Issue Display:
- Volume 19, Issue 2 (2014)
- Year:
- 2014
- Volume:
- 19
- Issue:
- 2
- Issue Sort Value:
- 2014-0019-0002-0000
- Page Start:
- 112
- Page End:
- 125
- Publication Date:
- 2013-12-10
- Subjects:
- Cytogenetics -- Periodicals
Cells -- Mechanical properties -- Periodicals
Molecular genetics -- Periodicals
Genes -- Periodicals
Molecular biology -- Periodicals
Cytology -- Periodicals
Biomechanics -- Periodicals
571.6 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-2443 ↗
http://www.blacksci.co.uk/%7Ecgilib/jnlpage.bin?Journal=GTC&File=GTC&Page=aims ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/gtc.12118 ↗
- Languages:
- English
- ISSNs:
- 1356-9597
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4111.762500
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 3199.xml