ArticleDrug design, development and therapy2026
Preliminary Exploration of Fluvastatin Inhibiting Proliferation, Migration and Invasion of Lung Cancer Cells and Reversing Paclitaxel Resistance: Mechanism Exploration Based on Multi-Omics Analysis.
Article in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Lung cancer is one of the leading causes of cancer-related deaths, among which NSCLC accounts for approximately 80-85% of all lung cancer cases. Paclitaxel (TAX) is a commonly used chemotherapeutic drug, but it is easy to cause drug resistance. Fluvastatin has anti-cancer potential, but the mechanism of its reversal of drug resistance is unclear. Methods: The study was divided into four groups: the A549 control group, the A549/Tax control group, the A549 Fluvastatin-treated group, and the A549/Tax Fluvastatin-treated group. CCK-8, Transwell, and flow cytometry assays were used to detect fluvastatin's effects on cell proliferation, migration, invasion, and apoptosis. Transcriptomics, proteomics, and acetylomics were combined to explore the potential molecular mechanisms. Results: The preliminary results showed that fluvastatin inhibited the proliferation, migration and invasion of A549 and A549/Tax cells and promoted their apoptosis. Multi-omics analysis revealed that a large number of differentially expressed molecules were detected in both the A549-Fluvastatin vs A549-NC group and the A549/Tax-Fluvastatin vs A549/Tax-NC group, and these molecules were significantly enriched in multiple biological processes and signaling pathways. This suggests that fluvastatin may exert its effects through the synergistic regulation of multiple molecules and pathways. Integrated multi-omics analysis identified several key molecules (for example, HMGCR, RDH11, HSPB1) and acetylated protein-target gene pairs (for example, P09874-BCL2, P42224-PTGS2, P04150-CCND3), which may mediate the antitumor mechanism of fluvastatin. Conclusion: This study indicates that fluvastatin has the potential to reverse TAX resistance in lung cancer, and the results of multi-omics analysis provide a theoretical basis for the exploration of potential therapeutic targets in the future.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.