ArticleFrontiers in pharmacology2025
From COPD to cancer: indacaterol's unexpected role in combating NSCLC.
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 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.
- SLC16A3 as an immunosuppressive Kupffer cell marker predicts poor prognosis in HBV-positive hepatocellular carcinoma.Journal of translational medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Non-small cell lung cancer (NSCLC) is one of the most prevalent and deadly malignancies worldwide. In previous studies, indacaterol, a drug used to manage chronic obstructive pulmonary disease, has shown antitumor activity. However, its role in the context of NSCLC remains underexplored. This study aimed to investigate indacaterol's mechanisms and potential therapeutic effects in lung cancer treatment. Methods: Expression profiles and clinical information from the TCGA database were analyzed to explore the potential impact of the Results: Analysis of TCGA data revealed that GLUT1 has a potential role in promoting NSCLC and may work in concert with MCT4. Indacaterol significantly inhibited the viability of NSCLC cells in a concentration-dependent manner. Molecular modeling and CETSA experiments further indicated that indacaterol may bind to GLUT1 and affect GLUT1 expression. Immunohistochemistry suggested that indacaterol also reduces the expression of MCT4, suggesting its potential to diminish the capacity of tumors to reprogram stromal metabolism. Conclusion: Indacaterol, a potential inhibitor of GLUT1, has significant antitumor effects on NSCLC. Moreover, the combination of indacaterol with immune checkpoint inhibitors may further enhanced the inhibitory effects of indacaterol on NSCLC cells. Our study provides scientific evidence supporting the clinical application of indacaterol as a novel therapeutic strategy for NSCLC treatment.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.