ArticleiMetaOmics2026
Integrin α5β1-mediated multicellular crosstalk in the tumor microenvironment drives bladder cancer progression and reveals targetable vulnerabilities.
Article in iMetaOmics, 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
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer (BCa) progression is driven by complex interactions within the tumor microenvironment, yet the underlying multicellular communication networks remain poorly defined. Here, we integrated bulk, single-cell, and spatial transcriptomic data with multiplexed immunofluorescence to construct a comprehensive cellular atlas across normal urothelium, precancerous lesions, and progressive BCa. We identified a stemness-associated malignant epithelial population (Cluster 1_SDC1), a prognostically unfavorable subset of POSTN+ myofibroblastic cancer-associated fibroblasts (mCAFs), and immunosuppressive monocytic myeloid-derived suppressor cells (M-MDSCs), all enriched in high-grade tumors. Spatial mapping revealed a coordinated signaling cascade wherein POSTN+ mCAFs and M-MDSCs co-localize and engage integrin α5β1 on tip endothelial cells through FN1 and NAMPT, collectively driving angiogenesis. In turn, tip endothelial cells reinforce tumor stemness through downstream COL4A1/2-SDC1 signaling. Therapeutically, targeting integrin α5β1 with RGD peptide suppressed tumor growth and vascularization, while its combination with hydrogel-based delivery and immune checkpoint blockade elicited broad-spectrum antitumor responses. These findings uncover a spatially coordinated immune-stroma-tumor signaling cascade and establish integrin α5β1 as a central therapeutic target, providing a rationale for stroma-directed combination strategies in progressive BCa.
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.