ArticleAsian Pacific journal of cancer prevention : APJCP2026
Dysregulated TMPO-AS1/let-7b-5p/PLK1/E2F1 Axis Associated with Poor Prognosis in Lung Adenocarcinoma.
Article in Asian Pacific journal of cancer prevention : APJCP, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesThis study examines the regulatory mechanisms underlying PLK1 overexpression in lung adenocarcinoma, especially in smokers. It focuses on understanding the ceRNA network, including mRNAs, miRNAs, and lncRNAs, while also identifying potential prognostic biomarkers.
methodsPublicly available databases, including Oncomine, TIMER 2.0, UALCAN, OncoMX, GEPIA2, OncoDB, ENCORI, KM Plotter, CellTracer, miRNet, CancerMIRNome, and Enrichr, were extensively utilized to assess the expression profile, prognostic significance, and regulatory interactions of PLK1 in lung adenocarcinoma (LUAD) and normal tissues.
resultsPLK1 expression is significantly elevated in lung adenocarcinoma (LUAD), with a hazard ratio of 1.95, indicating a correlation with poor overall survival. Among patients who smoke, elevated PLK1 expression is associated with a higher hazard ratio of 1.64 and reduced survivability. The transcription factor E2F1 has been identified as a potential regulator of PLK1 expression in LUAD. Additionally, the microRNA hsa-let-7b-5p shows a negative correlation with both E2F1 and PLK1, while the long non-coding RNA TMPO-AS1 is positively associated with the E2F1/PLK1 axis. These findings suggest a regulatory cascade where TMPO-AS1 may function as a molecular sponge for hsa-let-7b-5p, thereby enhancing E2F1-mediated PLK1 expression and promoting the progression of LUAD.
conclusionThe study highlights the PLK1/E2F1/hsa-let-7b-5p/TMPO-AS1 regulatory axis as a key contributor to aggressive LUAD. Targeting this ceRNA network either by inhibiting TMPO-AS1 or restoring hsa-let-7b-5p activity may offer a promising strategy for therapeutic intervention in smoking-associated LUAD.
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