LAMTOR5-AS1 predicts poor prognosis and regulates glioma progression via miR-4653-5p/TCF7 axis.

Gliomas, the most prevalent primary malignant brain tumors, are characterized by highly invasive growth patterns. Emerging evidence indicates that long non-coding RNAs are essential for regulating key oncogenic pathways. This study focuses on lncRNA LAMTOR5 antisense RNA AS1 (LAMTOR5-AS1, also known as SLC16A4-AS1), seeking to elucidate its regulatory functions in gliomas and assess its potential as a prognostic biomarker. LAMTOR5-AS1 expression in normal brain tissues and glioma samples was assessed using quantitative real-time polymerase chain reaction (qRT-PCR). The Cancer Genome Atlas (TCGA) glioma dataset was mined for COX regression and Kaplan-Meier survival analyses to check LAMTOR5-AS1 correlation with clinical outcomes. The competing endogenous RNA (ceRNA) function of LAMTOR5-AS1 targeting miR-4653-5p was determined using anti-AGO2 immunoprecipitation assays and dual-luciferase reporter assays. The oncogenic properties of LAMTOR5-AS1 in glioma were systematically detected through in vivo and in vitro phenotype experiments. The results revealed that glioma tissues had higher levels of LAMTOR5-AS1 expression, which had a positive correlation with glioma grade and indicated a poor outcome. LAMTOR5-AS1 knocking down inhibits the malignant progression of glioma cells. Mechanistically, it was demonstrated that the LAMTOR5-AS1 regulates TCF7 level via sponging miR-4653-5p, which was correlated with the malignant progression of glioma cells. To conclude, through the miR-4653-5p/TCF7 axis, LAMTOR5-AS1 serves as ceRNA and modulates the progression of glioma.