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Background <p>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 <i>RASL12</i> in LUAD progression.</p> Methods <p>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 <i>RASL12</i> knockdown, and rescue assays. Interactions were validated by dual-luciferase assays. Downstream pathways were explored via Gene Set Enrichment Analysis (GSEA).</p> Results <p>miR-6791-5p was significantly upregulated in LUAD (<i>p</i> &lt; 0.001), independently predicting poor overall survival (HR = 2.411, <i>p</i> = 0.003). Functionally, miR-6791-5p promoted LUAD cell proliferation, migration, and invasion. <i>RASL12</i> was confirmed as a direct target, exhibiting decreased mRNA and protein expression in tumors that negatively correlated with miR-6791-5p. Independent <i>RASL12</i> 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.</p> Conclusions <p>miR-6791-5p acts as an oncogene in LUAD by directly targeting the tumor suppressor <i>RASL12</i>. This axis modulates malignant phenotypes, representing a promising prognostic biomarker and potential therapeutic candidate.</p>

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Targeting RASL12 by miR-6791-5p fuels malignant progression in lung adenocarcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月25日

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  • Lu Zhang,
  • Zhonghao Pang,
  • Haibo Zhang,
  • Pin Wang

摘要

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.