Present address: Department of Chemical and Biomolecular Engineering, The Johns Hopkins University, Baltimore, Maryland, USA.
GM3 suppresses anchorage-independent growth via Rho GDP dissociation inhibitor beta in melanoma B16 cells
Article first published online: 31 MAY 2011
© 2011 Japanese Cancer Association
Volume 102, Issue 8, pages 1476–1485, August 2011
How to Cite
Wang, P., Xu, S., Wang, Y., Wu, P., Zhang, J., Sato, T., Yamagata, S. and Yamagata, T. (2011), GM3 suppresses anchorage-independent growth via Rho GDP dissociation inhibitor beta in melanoma B16 cells. Cancer Science, 102: 1476–1485. doi: 10.1111/j.1349-7006.2011.01963.x
- Issue published online: 18 JUL 2011
- Article first published online: 31 MAY 2011
- Accepted manuscript online: 25 APR 2011 06:59AM EST
- (Received January 31, 2011/Revised April 14, 2011/Accepted April 17, 2011/Accepted manuscript online April 25, 2011/Article first published online June 1, 2011)
Fig. S1. GM3 induces phosphorylation of Akt in mouse melanoma B16 cells.
Fig. S2. GM3 partially blocked the effects of Akt1/2 siRNA on colony formation in soft agar.
Fig. S3. Rictor knockdown inhibits phosphorylation of Aktser473 and induces colony formation, but did not block the effects of GM3 on the stimulating activity of Akt.
Fig. S4. Growth curves of St3gal5, Pdpk1, Raptor and Ly-GDI knockdown of cell lines in serum-deprived conditions.
Fig. S5. Effects of Ly-GDI knockdown on the expression of Rho family genes.
Table S1. GM3 involved in tumor-related gene regulation.
Table S2. Ly-GDI expression and the number of colonies in soft agar in different siRNA-treated B16 cells.
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