Hereditas · 2026
Targeting RASL12 by miR-6791-5p fuels malignant progression in lung adenocarcinoma.
СтатьяНазвание и аннотация: Перевод в очереди
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Zhang Lu, Pang Zhonghao, Zhang Haibo, Wang Pin
Аннотация
BACKGROUND: Lung adenocarcinoma (LUAD) poses significant clinical challenges due to its heterogeneity and metastatic potential, necessitating deeper molecular characterization. This study investigated the role of miR-6791-5p and its target RASL12 in LUAD progression.
METHODS: Expression profiles and prognostic relevance were analyzed in 203 LUAD patients, cell lines, and public databases. Biological functions were evaluated through CCK-8, Transwell, independent RASL12 knockdown, and rescue assays. Interactions were validated by dual-luciferase assays. Downstream pathways were explored via Gene Set Enrichment Analysis (GSEA).
RESULTS: miR-6791-5p was significantly upregulated in LUAD (p < 0.001), independently predicting poor overall survival (HR = 2.411, p = 0.003). Functionally, miR-6791-5p promoted LUAD cell proliferation, migration, and invasion. RASL12 was confirmed as a direct target, exhibiting decreased mRNA and protein expression in tumors that negatively correlated with miR-6791-5p. Independent RASL12 knockdown enhanced tumor aggressiveness, while its co-knockdown partially reversed the tumor-suppressive effects of miR-6791-5p inhibition. GSEA linked this axis to cell adhesion signaling dynamics.
CONCLUSIONS: miR-6791-5p acts as an oncogene in LUAD by directly targeting the tumor suppressor RASL12. This axis modulates malignant phenotypes, representing a promising prognostic biomarker and potential therapeutic candidate.
METHODS: Expression profiles and prognostic relevance were analyzed in 203 LUAD patients, cell lines, and public databases. Biological functions were evaluated through CCK-8, Transwell, independent RASL12 knockdown, and rescue assays. Interactions were validated by dual-luciferase assays. Downstream pathways were explored via Gene Set Enrichment Analysis (GSEA).
RESULTS: miR-6791-5p was significantly upregulated in LUAD (p < 0.001), independently predicting poor overall survival (HR = 2.411, p = 0.003). Functionally, miR-6791-5p promoted LUAD cell proliferation, migration, and invasion. RASL12 was confirmed as a direct target, exhibiting decreased mRNA and protein expression in tumors that negatively correlated with miR-6791-5p. Independent RASL12 knockdown enhanced tumor aggressiveness, while its co-knockdown partially reversed the tumor-suppressive effects of miR-6791-5p inhibition. GSEA linked this axis to cell adhesion signaling dynamics.
CONCLUSIONS: miR-6791-5p acts as an oncogene in LUAD by directly targeting the tumor suppressor RASL12. This axis modulates malignant phenotypes, representing a promising prognostic biomarker and potential therapeutic candidate.