Triptolide suppresses melanoma cell growth in vitro and in vivo through the Src-ERK signaling pathway.

Abstract

Melanoma is a highly aggressive form of skin cancer with a rapidly increasing incidence. New strategies are urgently needed for treating advanced melanoma which is closely linked to metastasis and often results in death. The Src-ERK signaling axis contributes significantly to both cell growth and metastasis. Triptolide, a Tripterygium wilfordii extract used for treating autoimmune conditions in traditional Chinese medicine, also has anti-inflammatory, neuroprotective, and antitumor activities. However, its ability to treat melanoma, including its target and underlying mechanism, requires clarification. We performed a range of in vivo and in vitro cellular experiments, encompassing assessments of cell proliferation, cell cycle progression, apoptosis, migration, and invasion, alongside nude mouse xenograft tumor studies, to evaluate the therapeutic potential of triptolide in melanoma. Here, it was found that triptolide markedly reduced proliferation, invasion, and migration in SK-MEL-5 and SK-MEL-28 cells. Triptolide was shown to arrest the cell cycle in G0/G1 and induce apoptosis, with further investigation showing that these effects were mediated by the Src-ERK pathway. Thus, the findings indicated that triptolide could inhibit melanoma cell growth and metastasis, suggesting its potential for treating metastatic melanoma.