Abstract
This study investigates the role of the long noncoding RNA (lncRNA) ZNF197-AS1 in uveal melanoma (UM), focusing on its function within a competing endogenous RNA (ceRNA) network. Using the UM-related TCGA (The Cancer Genome Atlas) dataset, we analyzed the expression levels of ZNF197-AS1 and its correlation with miR-425 and GABARAPL1, an essential autophagy-related gene. Our analysis revealed that ZNF197-AS1 acts as a ceRNA by competitively binding to miR-425, resulting in the upregulation of GABARAPL1. This interaction plays a crucial role in the growth and metastasis of UM. The expression of GABARAPL1 showed a strong correlation with the clinical outcomes of patients with UM. Furthermore, in vitro assays confirmed that ZNF197-AS1 impedes UM cell proliferation, migration, and invasion by modulating the miR-425/GABARAPL1 axis. These findings suggest that ZNF197-AS1 can effectively inhibit UM progression through this ceRNA regulatory network. This study provides valuable insights into the molecular mechanisms underlying UM and highlights the potential of targeting the ZNF197-AS1/miR-425/GABARAPL1 axis as a therapeutic strategy for UM.NEW & NOTEWORTHY This study identifies the ZNF197-AS1/miR-425/GABARAPL1 axis as a novel regulatory mechanism in uveal melanoma. ZNF197-AS1 upregulates GABARAPL1 by sponging miR-425, inhibiting UM cell proliferation, migration, and invasion. This discovery highlights a potential therapeutic target, providing new insights into UM progression and patient outcomes.