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. 2010 Mar 15;120(4):1165–1177. doi: 10.1172/JCI40582

Figure 2. Expression of RSK2 promotes in vitro HNSCC cell invasion.

Figure 2

(A) Enforced expression of RSK2 resulted in increased invasive ability in poorly metastatic HNSCC cells, including 686LN, Tu212, and 37A, in the in vitro Matrigel invasion assay. Relative invasion was normalized to the invasion of control cells without transfection (mean ± SD). **P < 0.01, by 2-tailed Student’s t test. (B) Treatment with RSKI-fmk (6 μM) effectively decreased RSK2 kinase activity, as assessed by phosphorylation level of S386, in RSK2-expressing M4e, 212LN, and 37B cells. (C) Representative areas show that inhibition of RSK2 by RSKI-fmk treatment decreased the numbers of M4e and 212LN cells that crossed the Matrigel in the invasion assay. Original magnification, ×50. (D and E) Inhibition of RSK2 by RSKI-fmk (D) or BI-D1870 (E) (6 μM) decreased invasive ability of M4e, 212LN, and 37B cells. Relative invasion was normalized to the invasion of control cells without drug treatment (mean ± SD; *P = 0.01–0.05). (F) Targeting RSK2 by RSKI-fmk or BI-D1870 (6 μM) did not significantly affect the proliferation rate of M4e, 212LN, and 37B cells (mean ± SD). Cell number of each sample was determined by normalizing the cell viability to that of a standard curve of cell number.