ArticleRespiratory research2026
The Wnt receptor Frizzled3 (FZD3) drives aggressive phenotypes in small cell lung cancer.
Article in Respiratory research, 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSmall cell lung cancer (SCLC) is an aggressive neuroendocrine malignancy characterized by rapid progression and poor prognosis. This study integrates bioinformatics with experimental validation to characterize the role of Frizzled-3 (FZD3), a Wnt receptor, in SCLC progression.
methodsWe analyzed transcriptomic data from 102 SCLC and 55 normal lung tissues retrieved from the Gene Expression Omnibus (datasets GSE6044, GSE40275, and GSE60052). Differential expression analysis was performed using the limma package, followed by GO and KEGG pathway enrichment analyses. To screen for robust prognostic markers, we employed machine learning algorithms-specifically LASSO and Random Forest-to select hub genes. The prognostic significance of FZD3 was assessed using multivariate Cox regression and Kaplan-Meier survival analysis. Validation assays, including qRT-PCR, Western blotting, and functional assays (proliferation, migration, invasion, and apoptosis), were conducted in SCLC cell lines and clinical specimens.
resultsA total of 1,192 differentially expressed genes were identified. Enrichment analysis revealed significant involvement in immune-related pathways and Wnt signaling. FZD3 was selected as a key hub gene and found to be upregulated in SCLC tissues and cell lines. High FZD3 expression was correlated with advanced clinical stage(by Kruskal-Wallis test), and poor prognosis (by Survival analysis). In vitro function assays demonstrated that FZD3 knockdown significantly attenuated SCLC cell proliferation, migration, and invasion while inducing apoptosis.
conclusionFZD3 is frequently overexpressed in SCLC and serves as an independent prognostic indicator for poor survival. Our findings elucidate the oncogenic role of FZD3 in SCLC, highlighting its potential as a therapeutic target and prognostic biomarker.
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.