Abstract:

Cutaneous melanoma (CM) is a highly malignant tumor caused by malignant proliferation of melanocytes, characterized by distant metastasis and high mortality. Although targeted therapy and immunotherapy have significantly improved the survival rates of advanced CM patients, tumor resistance remains a key barrier to further improving treatment outcomes. In recent years, significant progress has been made in the study of autophagy as a key regulatory cell death mode in the pathogenesis of CM. Autophagy is the main mechanism that mediates the degradation and recycling of various cellular components through lysosomes to maintain the homeostasis of the intracellular environment. A large number of studies have confirmed that the role of autophagy in CM is complex and controversial. In the early stages of CM development, autophagy may inhibit abnormal proliferation of tumor cells by removing damaged cell components. However, as the tumor progresses, autophagy may transform into a role that promotes tumor invasion and metastasis. In advanced CM, the activation of autophagy helps tumor cells survive in stressful environments. In particular, in CM with BRAF (V-Raf murine sarcoma viral oncogene homolog B1) mutations, autophagy activity is often enhanced, weakening the effectiveness of BRAF inhibitor-targeted therapy. This article provides an in-depth analysis of the dual effects of autophagy on the progression of CM and explores the role of autophagy in CM resistance, in order to provide insights for the development of new targeted therapy strategies for CM.

Key words: cutaneous melanoma, autophagy, autophagy-related protein (ATG), targeted therapy