Identification of hub gene and lncRNA signature related to entotic cell death in cutaneous melanoma for prognostic and immune prediction

Entotic cell death (ECD), a cell death program observed in cancer cell competition, predominantly occurs in an autophagy protein-dependent, non-apoptotic manner. However, the relationship between cutaneous melanoma (CM) and ECD-associated genes and lncRNAs has remained unclear. This study aimed to elucidate the role and mechanism of ECD-associated genes in CM. To achieve this, 4 mechanism learning algorithms and integrated bioinformatic analyses were employed to identify the core ECD-associated genes and lncRNAs. Subsequently, 2 risk signatures based on ECD-associated genes and hub lncRNAs were constructed for CM patients. As a result, we observed significant differential expression of ECD-associated genes in CM, indicating their potential as valuable predictors for CM patients. Moreover, RHOA was identified as a core ECD-associated gene in CM, and its expression was found to be associated with patients’ survival and immune infiltration, suggesting its relevance as a potential therapeutic target. Additionally, this study provided clarification on hub ECD-associated lncRNAs in CM, offering insights into their roles in the disease. Through bioinformatic analyses, we identified 2 risk signatures based on the expression of ECD-associated genes and hub ECD-associated lncRNAs, respectively. Both risk signatures were strongly linked to the prognosis and cancer growth of CM, underscoring their potential as valuable prognostic indicators. Furthermore, mechanistic analyses suggested a significant association between the risk signature and the immune microenvironment in CM, highlighting potential immune-related implications in disease progression. In conclusion, we propose that ECD-associated genes and lncRNAs hold promise as potential targets in CM. Moreover, our findings revealed a significant correlation between ECD and the immune microenvironment, providing crucial insights for guiding individualized treatment strategies in CM.