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. 2018 Jan 17;17(3):4203–4212. doi: 10.3892/mmr.2018.8444

Figure 5.

Figure 5.

Tunicamycin regulates growth and apoptosis of clonal tumor cells through the ERK-JNK-mediated AKT/mTOR signaling pathway. (A) Tunicamycin inhibits total and phosphorylated AKT expression in SW620 cells. (B) Tunicamycin inhibits mTOR expression in SW620 cells. Effects of ERK overexpression on expression of (C) total and phosphorylated AKT and (D) mTOR in SW620 cells. (E) Tunicamycin blocked ERK overexpression-induced growth and (F) ERK overexpression-inhibited apoptosis in SW620 cells. Data are expressed as the mean ± standard deviation of triplicate experiments. **P<0.01. ERK, extracellular signal-regulated kinase; JNK, c-JUN N-terminal kinase; tAKT, total AKT; pAKT, phosphorylated AKT; mTOR, mechanistic target of rapamycin; ERKOR, ERK overexpression.