ZNF197-AS1/miR-425/GABARAPL1 axis: a novel regulatory mechanism in uveal melanoma

This study investigates the role of the long noncoding RNA (lncRNA) <i>ZNF197-AS1</i> 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 <i>ZNF197-AS1</i> and its correlation with <i>miR-425</i> and <i>GABARAPL1</i>, an essential autophagy-related gene. Our analysis revealed that <i>ZNF197-AS1</i> acts as a ceRNA by competitively binding to <i>miR-425</i>, resulting in the upregulation of <i>GABARAPL1</i>. This interaction plays a crucial role in the growth and metastasis of UM. The expression of <i>GABARAPL1</i> showed a strong correlation with the clinical outcomes of patients with UM. Furthermore, in vitro assays confirmed that <i>ZNF197-AS1</i> impedes UM cell proliferation, migration, and invasion by modulating the <i>miR-425/GABARAPL1</i> 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 <i>ZNF197-AS1/miR-425/GABARAPL1</i> axis as a therapeutic strategy for UM.<b>NEW & NOTEWORTHY</b> 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.