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Updated: Jun 2, 2026
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Effect of vegf gene knockdown on growth of the murine sarcoma cell line MS-K
Xiu Y Zhong1, Asami Yoshioka, Yuka Mashio
1Department of Cell Science, Faculty of Graduate School of Science and Technology, Niigata University, Nishi-ku, Niigata 950-2181, Japan.
Abstract:
The murine sarcoma cell line MS-K was previously established as a Ki-ras-positive cell line. Inoculation of this cell line under the flank of C3H/HeN mice results in the growth of large tumors with well-developed blood vessels within day 30 of transplantation without any metastasis because MS-K cells produce vascular endothelial growth factor (VEGF). To elucidate the role of VEGF in tumor formation in vivo, stable vegf-knockdown-MS-K clones were obtained using plasmid-based knockdown vectors. Interestingly, tumorigenesis was completely suppressed in a vegf-A-knockdown-MS-K clone [designated MS-K (A-KD)]. Proliferation and colony formation capacity of the MS-K (A-KD) cells in a semi-solid medium under low serum conditions was significantly lower than that of control MS-K (SCR) cells; however, the expression of vegf-receptor 1 (vegf-r-1) was not changed. Addition of the recombinant VEGF-A(165) partially restored the colony formation capacity of MS-K (A-KD) cells and caused the phosphorylation of VEGF-r-1 (Flt-1) in MS-K (Normal) cells. Furthermore, tumorigenicity of the vegf-r-1-knockdown-MS-K clone [designated MS-K (R1-KD)] had obviously delayed or strongly suppressed compared with the MS-K (Normal). These results indicate that Vascular endothelial growth factor-A, produced from MS-K, acts as a growth factor for MS-K cells itself and supports tumor formation in vivo by inducing the blood vessel formation.
Insights
Vascular Endothelial Growth Factor-A (VEGF-A) produced by MS-K sarcoma cells promotes tumor growth by stimulating blood vessel formation and acting as an autocrine growth factor. Suppressing VEGF-A or its receptor VEGFR-1 inhibits tumor development.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- MS-K murine sarcoma cells are Ki-ras-positive and produce vascular endothelial growth factor (VEGF).
- MS-K cell inoculation in mice leads to rapid tumor growth with neovascularization but no metastasis.
- The role of VEGF in MS-K tumor formation requires further elucidation.
Purpose of the Study:
- To investigate the role of VEGF in MS-K tumor formation in vivo.
- To determine if VEGF acts as an autocrine growth factor for MS-K cells.
- To assess the impact of VEGF receptor 1 (VEGFR-1) on MS-K tumorigenesis.
Main Methods:
- Generation of stable vegf-A-knockdown (MS-K (A-KD)) and vegf-r-1-knockdown (MS-K (R1-KD)) MS-K cell clones using plasmid-based vectors.
- Assessment of tumor formation, cell proliferation, and colony formation capacity in vitro and in vivo.
- Analysis of VEGF receptor 1 (VEGFR-1) expression and phosphorylation.
Main Results:
- Tumorigenesis was completely suppressed in MS-K (A-KD) cells.
- MS-K (A-KD) cells exhibited significantly reduced proliferation and colony formation under low serum conditions.
- Recombinant VEGF-A(165) partially restored colony formation in MS-K (A-KD) cells and induced VEGFR-1 phosphorylation in MS-K (Normal) cells.
- Tumorigenicity was significantly delayed or suppressed in MS-K (R1-KD) cells.
Conclusions:
- VEGF-A produced by MS-K cells functions as an autocrine growth factor, promoting MS-K cell proliferation and colony formation.
- VEGF-A supports tumor formation in vivo by inducing blood vessel formation.
- VEGFR-1 signaling is crucial for MS-K tumor development.
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