ArticlePloS one2026
Regulatory effects of smoking cessation on the cellular microenvironment and differentially expressed genes in precancerous lesions of pulmonary nodules in mice based on single-cell RNA sequencing and immune repertoire-sequencing.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSmoking cessation decreases lung cancer progression; however, its effects on precancerous lesions and the underlying mechanisms remain unclear. This study established a mouse model of precancerous pulmonary nodules and employed single-cell RNA sequencing (scRNA-seq) and immune repertoire sequencing (IR-seq) to elucidate the regulatory mechanisms by which smoking cessation influences the development of lung precancerous lesions.
methodsA B[a]P-induced mouse model of pulmonary precancerous lesions was established after 6 weeks of B[a]P treatment. Lung nodules were identified via micro-MRI, and histopathological features were assessed by H&E staining. After confirming the establishment of precancerous lesions in smoking-exposed mice, graded B[a]P withdrawal for 4 and 8 weeks was implemented. Nodule size was measured using Generic Medical Imaging software. scRNA-seq and IR-seq analyzed immune cell composition, proportions, signaling, and gene expression.
resultsB[a]P withdrawal reduced new lung nodule formation and decreased the diameter, area, and volume of existing nodules. It alleviated cellular atypia, reduced inflammation, and altered the tumor microenvironment by increasing T-, B-, and NK cells while reducing monocytes and neutrophils. Concurrently, B[a]P withdrawal downregulated Vim, GPX1, Atf3, CD44, and Arpc5 and upregulated Hsph1, Hsp90aa, and Hspa1b. B[a]P withdrawal upregulated CD80 and ICOS, suppressed intercellular communication via Icam1-(Itgal+Itgb2), Ppia-Bsg, and Thbs1-Cd47 pathways. The APP-CD74 pathway emerged as a novel regulator in precancerous lesions. IR-seq revealed restored T- and B-cell receptor diversity, CDR3 sequence alterations, and V(D)J gene regulation.
conclusionsB[a]P withdrawal reduces lung nodules, inhibits progression, potentially by enhancing immune surveillance by modulating immune cells, signaling pathways, and gene expression, while promoting ferroptosis, suppressing inflammation, and preventing tumor stem cell-like traits. These findings may provide mechanistic insights into the beneficial effects associated with smoking cessation.
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.