ArticleFrontiers in pharmacology2025
LncRNA OIP5-AS1 suppresses lung adenocarcinoma progression and modulates macrophage polarization through the miR-429/DOCK4 regulatory axis.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Elevated DOCK4 expression correlates with favorable prognosis and immune infiltration in clear cell renal cell carcinoma.Annals of medicine · 2026Article
- ING5-mediated regulation of lung cancer progression via the OIP5-AS1/miR-381-3p/SEC24A axis.Translational cancer research · 2025Article
- Investigating the Relationship Between Long Non-Coding RNAs and miR-200 Family Expression in Clear Cell Renal Cell Carcinoma.Cancers · 2025Article
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5 authors.
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Abstract
Background: Macrophage polarization plays a pivotal role in shaping the tumor microenvironment and influencing cancer progression. Long non-coding RNAs (lncRNAs) have emerged as important regulators of this process. This study investigated the role of lncRNA OIP5-AS1 in lung adenocarcinoma (LUAD) progression and its involvement in macrophage polarization. Methods: The expression of OIP5-AS1 in LUAD tissues and its association with patient prognosis were analyzed. Functional assays, including cell proliferation, migration, invasion, and cell cycle analysis, were conducted in LUAD cell lines. Bioinformatics prediction, luciferase reporter assays, and RNA immunoprecipitation (RIP) were used to explore the interaction among OIP5-AS1, miR-429, and DOCK4. Macrophage polarization and migratory capacity were assessed following manipulation of OIP5-AS1, miR-429, and DOCK4 expression. Results: OIP5-AS1 expression was significantly decreased in LUAD tissues and associated with poor survival. Overexpression of OIP5-AS1 inhibited LUAD cell proliferation, migration, and invasion, induced G1 phase arrest, and suppressed tumor growth Conclusion: OIP5-AS1 modulates macrophage polarization through the miR-429/DOCK4 axis and inhibits LUAD cell progression. This regulatory pathway may influence the tumor immune microenvironment and represent a potential therapeutic target in LUAD.
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