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. 2015 Aug 29;1:116–125. doi: 10.1016/j.pvr.2015.08.001

Fig. 6.

Fig. 6.

Silencing of K-ras, a miR-181a/d target, inhibits anchorage independent growth and migration ability in HPV16-transfected OSCC cells. (A) Decreased expression of K-ras in HPV16-tranfected OSCC cell lines was determined by Western blot analysis. GAPDH was used as controls. (B) Ectopic expression of miR-181a, miR-181d, and miR-181a/d decreased K-ras in UM6/HPV16 as determined by Western blot analysis. (C) Endogenous K-ras in UM6/HPV16 was knocked down using siRNA against K-ras (K-ras siRNA). The cells transfected with control siRNA (CTLi) were included for comparison. (D) Effect of K-ras knockdown on anchorage independent growth in UM6/HPV16 was determined by soft agar assay. ⁎P<0.05 by two-tailed Student’s t test. (E) Effect of K-ras knockdown on migration ability of UM6/HPV16 was determined by transwell migration assay. ⁎P<0.05 by two-tailed Student’s t test. Representative images of transwell migration assay from UM6/HPV16 transfected with CTLi and K-ras siRNA are shown on the right side. (F) Effect of K-ras knockdown on self-renewal capacity of UM6/HPV16 was determined by tumor sphere formation assay.