ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Integrated bioinformatics analyses and cell line experiments implicate miR-33a-5p/HIF1A in the cellular response to celastrol in lung adenocarcinoma.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
8 authors.
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Abstract
Celastrol has reported antitumor effects in lung cancer, but database-derived target lists and pathway predictions vary with the filters used. We examined which findings remained supported after evidence review and then tested the leading miRNA-target relationship in lung adenocarcinoma (LUAD) cells. Celastrol-associated proteins were curated from CTD and ChEMBL. Candidate miRNAs were reassessed by a reproducible literature search and an independent TCGA-LUAD screen. Alternative miRNA-target and disease-expression rules were compared. Network, enrichment, prognosis, monotherapy sensitivity, and structure analyses were retained as secondary analyses. A549 and H1975 cells were used for viability, qRT-PCR, HIF1A 3'UTR reporter, and miR-33a-5p inhibitor-rescue assays. Twenty-three proteins met the activity-based target rule; five had a retained direct binding measurement. The strict target/miRNA-target/LUAD differential-expression intersection was empty. Under an FDR-only disease rule, HIF1A was retained by four of five miRNA-target definitions but not by the ≥ 2-source rule. HIF1A expression was higher in GSE10072 LUAD tumors than in normal lung (log2 fold change = 0.566; Wilcoxon P = 4.24 × 10
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Registered trials
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