ArticleFunctional & integrative genomics2026
Single-cell and spatial transcriptomics identify CAPG as a key driver of cisplatin resistance in bladder cancer.
Article in Functional & integrative genomics, 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
8 authors.
Funding
Abstract
Cisplatin-based chemotherapy is widely used for bladder cancer, yet therapeutic resistance remains a major clinical obstacle. Here, by integrating cisplatin-related single-cell RNA sequencing datasets with spatial transcriptomics, we identified distinct malignant cell populations associated with cisplatin resistance. These resistant states exhibited enhanced stemness features, increased intercellular communication, and metabolic adaptation. Building on these resistance-associated cellular programs, we applied a cross-platform screening strategy incorporating urinary proteomics and transcriptomic profiling of cisplatin-resistant bladder cancer cells to prioritize clinically relevant resistance-associated genes. Through this approach, macrophage capping protein (CAPG) emerged as a key resistance-associated regulator. CAPG expression was consistently elevated in cisplatin-resistant tumors and cell models. Functional studies demonstrated that CAPG depletion suppressed malignant phenotypes, restored cisplatin sensitivity, and reduced IC
Indexed as
Identifiers
42479258What 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.