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. Author manuscript; available in PMC: 2013 Jul 18.
Published in final edited form as: Cancer Prev Res (Phila). 2009 Mar 31;2(4):370–376. doi: 10.1158/1940-6207.CAPR-08-0209

Fig. 3.

Fig. 3

Effect of myoinositol on endogenous and nicotine-induced P-Akt and P-ERK. A, top left, dose-dependent inhibition of Akt and ERK phosphorylation by myoinositol in immortalized HBECs, as assessed by immunoblotting; top right, effect of myoinositol pretreatment on nicotine-induced P-Akt and P-ERK in HBEC analyzed by immunoblotting. B, a PI3K inhibitor, a MEK inhibitor, and myoinositol all reduce proliferation in immortalized HBEC and HBEC(R) cells, but not in fully transformed H322 cells. HBEC, HBEC(R), or H322 cells were incubated with 15 μmol/L LY294002, 15 μmol/L U0126, or 5 mmol/L myoinositol. Left, immunoblots showing the effects of the compounds after 2 h; right, effect of compounds on cell proliferation after 72 h. Cell proliferation was normalized to vehicle-treated cells. The experiments were repeated thrice with triplicate samples.

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