LINC01123 drives autophagy-mediated promotion of ovarian tumor metastasis through the p65/ATG13 pathway

Long non-coding RNAs (lncRNAs) are increasingly recognized as critical regualtors in cancer biology, including ovarian cancer (OC). Analysis of the OC cohort in the Cancer Genome Atlas (TCGA) revealed that LINC011123 is significantly upregulated in OC compared to normal ovarian tissue. Nonetheless, the functional consequence of this upregulation and the underlying mechanism of LINC01123 in OC remain unclear. We hypothesized that elevated LINC01123 exerts an oncogenic function. RNA sequencing datasets from TCGA were analyzed to identify the RNAs with differential expression in OC tissues relative to standard ovarian tissue. The role of LINC01123 in regulating cell proliferation, migration, and autophagy was defined through functional experiments including wound healing, transwell, and western blotting in vitro , and a xenograft mouse model in vivo . LINC01123 regulation underwent investigation using RNA pulldown and mass spectrometry, RNA immunoprecipitation, luciferase reporter assays, and so on. LINC01123 is one of the most highly increased lncRNAs in OC specimens compared to non-cancerous ovarian tissue. Downregulation of LINC01123 functioned to suppress proliferation and cellular migration. RNA pulldown and gene set enrichment analysis suggested that the amount of LINC01123 positively correlated with genes involved in autophagy. LINC01123 promoted autophagy by promoting ATG13 expression. Further mechanistic studies showed that LINC01123 directly binds to p65 to activate ATG13 transcription, promoting autophagy and facilitating OC tumorigenesis. Our results uncovered the oncogenic function and mechanism of LINC01123 in OC. LINC01123 associates with p65, augmenting autophagy, which in turn facilitates tumor metastasis within OC cells by increasing ATG13 expression. LINC01123 is a potential therapeutic target for OC patients.