GS-168AT2 Inhibits Tumor Growth and Angiogenesis
Author Information
Author(s): Colin S, Guilmain W, Creoff E, Schneider C, Steverlynck C, Bongaerts M, Legrand E, Vannier J P, Muraine M, Vasse M, Al-Mahmood S
Primary Institution: Gene Signal Research Center
Hypothesis
The truncated form of CD9-partner 1 (CD9P-1), GS-168AT2, inhibits tumor-induced angiogenesis and tumor growth.
Conclusion
GS-168AT2 significantly inhibits angiogenesis and tumor growth by downregulating CD151 and CD9.
Supporting Evidence
- GS-168AT2 inhibited in vitro angiogenesis with an IC50 of 1.75±0.13 μM.
- GS-168AT2 reduced tumor growth by 73.9±16.4% in Calu-6 tumor xenografts.
- Treatment with GS-168AT2 led to significant downregulation of CD151 and CD9 on endothelial cells.
Takeaway
A new protein called GS-168AT2 can stop tumors from growing by blocking the formation of blood vessels that feed them.
Methodology
The study involved in vitro assays to measure the effects of GS-168AT2 on endothelial cell proliferation, migration, and angiogenesis, as well as in vivo experiments using tumor xenografts in mice.
Potential Biases
Potential bias may arise from the use of specific cell lines and animal models that may not fully represent human conditions.
Limitations
The study primarily focused on a single truncated form of CD9P-1 and its effects, which may not represent the full range of CD9P-1 functions.
Participant Demographics
Female BALB/c nu/nu mice were used in the in vivo experiments.
Statistical Information
P-Value
0.03
Confidence Interval
53.4±9.5%
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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