MARCH1 silencing inhibited tumour growth in nude mice via the down‐regulating of the PI3K/P‐AKT/β‐catenin pathways. A, Tumour growth curves for different therapy groups of PBS‐injected, negative siRNA‐injected and MARCH1‐injected tumours, respectively. B and C, Images of representative mice for different therapy groups. D, Tumour weight for different therapy groups. E, Protein expression of MARCH1, PI3K, AKT, P‐AKT, β‐catenin, MCL‐1, BCL‐2, Cleaved caspase‐3 and Cleaved caspase‐7 in the three different therapy tumour tissues with PBS‐injected, negative siRNA‐injected and MARCH1‐injected for four groups samples. F, Model for MARCH1 in PI3K/AKT/β‐catenin signalling. MARCH1 induces PI3K membrane recruitment, which activates phosphorylation and recruitment of AKT, leading to the promotion of β‐catenin expression. Subsequently, the phosphorylation and degradation of β‐catenin is decreased. AKT activation can trigger Mcl‐1 and Bcl‐2 up‐regulation, thus blocking the cytc/caspase‐3/7 pathway. All the data in this figure are represented as mean ± SD. *P < 0.05, **P < 0.01