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. Author manuscript; available in PMC: 2016 Jun 27.
Published in final edited form as: Mol Cancer Res. 2011 Oct 17;9(12):1644–1657. doi: 10.1158/1541-7786.MCR-11-0371

Figure 6. Twist1 induces growth arrest and is associated with a low ERK:p38 activity ratio.

Figure 6

(A) Cell counts in triplicate in a 24-well plate at indicated times from seeding of MCF10A cells transduced with a lentivirus expressing either the control luciferase, Twist1, or Twist2 shRNA, then treated with 2 ng/ml TGFβ1 continuously or transiently for 4h, and cell numbers determined at indicated times. Error bars represent mean +/− s.e.m. Representatives of 3 independent experiments are shown. (B and C) Western blotting for indicated proteins of WCL (B) from MCF10A cells similarly manipulated as in (A). The ratio of p-ERK1/2 normalized to total ERK1/2 over p-p38 normalized to total p38 was determined by densitometry (B) and shown as percent of the ratio in untreated control cells (C). Error bars represent mean +/− s.e.m. from 3 independent experiments. Student’s T-test, * p<0.05 for each comparison between Twist1 shRNA and each other experimental condition. (D) Schematic of a potential Twist1-p38-ERK signal feedback loop. Directions where direct evidence is provided are represented as solid lines. The p38 to Twist1 direction is proposed and shown as broken arrow. The p38 to ERK1/2 inhibitory crosstalk has been reported elsewhere. See also related Figure S10–S12.