Expression and clinical significance of MCF2L-AS1 in stomach adenocarcinoma

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.