Meanwhile, exogenous EP4 overexpression inhibited ERK1/2 phosphorylation, whereas exogenous DNMT1 overexpression antagonized the inhibitory effect of SM on c‐Jun protein expression, and the exogenous c‐Jun overexpression blocked the inhibitory effect of SM on lung cancer cells, thus inhibiting ERK1/2 phosphorylation. Here, JUN is linked to lung cancer.