ArticleJournal of cell communication and signaling2026
Rapid normal fibroblast-tumor crosstalk promotes cancer-associated fibroblast-like activation and attenuates mitomycin C cytotoxicity in bladder cancer.
Article in Journal of cell communication and signaling, 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
Normal fibroblasts (NFs) are among the earliest stromal cells encountered by bladder cancer cells during invasion into the lamina propria, yet their contribution to tumor progression and intravesical chemotherapy response remains poorly defined. Here, we investigated whether NFs are passive stromal bystanders or active participants in early bladder cancer microenvironmental remodeling. Analysis of an early-stage non-muscle-invasive bladder cancer transcriptomic cohort revealed that fibroblast-associated scores were higher in T1 than Ta tumors, enriched in European Organisation for Research and Treatment of Cancer high-risk disease, positively correlated with epithelial-mesenchymal transition (EMT) scores, and associated with increased expression of resistance-linked genes. Experimentally, fibroblast-conditioned medium reduced bladder cancer cell proliferation while accelerating wound closure, indicating a less proliferative but more motile phenotype. This was accompanied by EMT-like cadherin remodeling, including reduced E-cadherin and increased N-cadherin staining. Reciprocally, tumor-derived signals rapidly induced cancer-associated fibroblast (CAF)-like activation features in NFs within 48 h, including increased α-smooth muscle actin, fibroblast activation protein, and PDGFRβ expression. Functionally, increasing fibroblast-to-tumor cell ratios progressively attenuated mitomycin C (MMC)-induced cytotoxicity, demonstrating that stromal context can modify chemotherapy response in vitro. Together, these findings show that NF-tumor crosstalk is rapid, bidirectional and functionally relevant to MMC response in vitro. Rather than acting only after stable CAF formation, NFs can rapidly acquire CAF-like activation features following tumor-derived stimulation and contribute to a stromal context associated with EMT-like plasticity and reduced MMC-induced cytotoxicity in vitro.
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.