Abstract
BACKGROUND: Stomach Adenocarcinoma (STAD) poses a significant burden due to its high prevalence and costly, painful treatments, exerting considerable pressure on individuals. OBJECTIVES: This study intends to explore novel therapeutic targets to enhance prognosis and alleviate patient stress. MATERIALS AND METHODS: Quantitative Real-time Polymerase Chain Reaction was employed to detect MCF2L-AS1 expression in STAD tissues and cell lines. The correlation between this expression and patients' clinical conditions and prognosis was analyzed utilizing the Chi-squared test and Kaplan-Meier method. To investigate the regulatory mechanism of MCF2L-AS1, the Luciferase reporter gene system and transfection experiments were implemented. Cellular behaviors were analyzed through CCK8 and Transwell assays. RESULTS: MCF2L-AS1 expression was upregulated in STAD tissues and cells, strongly correlating with TNM stage and lymph node metastases. High MCF2L-AS1 levels were associated with reduced 5-year survival rates compared to the low-expression groups. miR-503-5p, a downstream miRNA, was downregulated in STAD and inversely correlated with MCF2L-AS1. Knockdown of MCF2L-AS1 suppressed miR-503-5p expression, indicating its role as a competitive endogenous RNA. Low miR-503-5p expression reversed the inhibitory effects of MCF2L-AS1 knockdown on STAD cell behaviors. CONCLUSIONS: The oncogene role of MCF2L-AS1 in STAD is mediated through the negative regulation of miR-503-5p, highlighting its potential as a prognostic marker and therapeutic target.