To explore the mechanisms of paclitaxel on melanoma and the role of the epidermal growth factor receptor (EGFR) signaling pathway in regulating the invasion and metastasis of melanoma, and to reveal the relationship between the EGFR signaling pathway and paclitaxel resistance of melanoma cells.

Using malignant melanoma A375 cells with high EGFR expression, we utilized flow cytometry, Transwell assay, MTT, and Western blot to study the effects of paclitaxel and epidermal growth factor (EGF) on A375 cell apoptosis, proliferation, and migration.

Paclitaxel induced apoptosis of A375 cells in a concentration-dependent manner (P＜0.001). Meanwhile, paclitaxel (0.1 μmol/L) inhibited Bcl-2 expression and increased the expression of Bax (P＜0.01). EGFR inhibitor AG1478 (20 μmol/L) could significantly increase the apoptosis of A375 cells and enhance the apoptosis-inducing effect of paclitaxel (P＜0.05) and its effect on Bcl-2 and Bax expression (P＜0.001). EGF treatment alone had no significant effect on the apoptosis of A375 cells, but it could inhibit the apoptosis-inducing effect of paclitaxel (0.1 μmol/L) as well as its effect on Bcl-2 and Bax (P＜0.001). Paclitaxel (0.1 μmol/L) inhibited the proliferation of A375 cells (P＜0.001), which could be further enhanced by AG1478 but was inhibited by EGF (P＜0.001). Paclitaxel (0.1 μmol/L) inhibited the migration of A375 cells (P＜0.001), which could be further enhanced by AG1478 but was decreased by EGF (P＜0.001).

Paclitaxel can reduce Bcl-2 expression but increase the expression of Bax, thereby inducing the apoptosis of melanoma A375 cells and inhibiting their proliferation and migration. However, these inhibitory effects can be weakened by EGF via the EGFR pathway.