Fig. 7

MYSM1 suppresses CRC tumorigenesis by inhibiting PI3K/AKT signaling. A Western blot analysis showing that PI3K/AKT signaling, as indicated by the expression of p-AKT (Ser473), p-AKT (Thr308), p-PDK1 (Ser241) and p-GSK-3β (Ser9), was stimulated in HCT116 cells (left) with MYSM1 knockdown and inhibited in SW620 cells (right) with MYSM1 overexpression, while PTEN presented the opposite trends. B The mRNA levels of PTEN and PHLPP1 in pretreated HCT116 and SW620 cells were analyzed by qRT-PCR. C and D The proliferation of HCT116 cells pretreated with siNC or siMYSM1 accompanied by DMSO, rapamycin (10 nmol/L) or wortmannin (100 nmol/L) as indicated for 48 h was examined by growth curve (C) and colony formation (D) assays. E and F Migration in pretreated HCT116 cells was determined via wound healing (E) and Transwell (F) assays. Scale bars: 50 μm. In B-F, the data are shown as the means ± SDs (*P < 0.05 and **P < 0.01, n = 3 independent experiments)