ArticleJournal of molecular histology2026
Cx43 modulates malignant phenotypes in bladder cancer cells via the c-Src/PTEN/FAK axis.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
- Mechanical stress, metabolic reprogramming and stromal remodeling: an emerging paradigm in the bladder cancer mechano-micro-environment.Frontiers in genetics · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Bladder cancer (BC), a leading urogenital malignancy with high mortality, lacks effective early biomarkers. Connexin 43 (Cx43), encoded by GJA1, regulates tumor growth via protein interactions and phosphorylation. While dysregulated in BC, Cx43's downstream regulatory pathways remain unclear. Elucidating these mechanisms is crucial for identifying novel biomarkers and therapeutic targets. qRT-PCR measured Cx43 expression in bladder cancer tissues and cells. Kaplan-Meier analysis assessed correlation between Cx43 expression and patient overall survival (OS) and progression-free survival (PFS). Using MTT, colony formation, and Transwell assays, we evaluated how silencing Cx43 affects BC cell proliferation, migration, and invasion in vitro. Protein-protein interaction (PPI) analysis predicted potential Cx43 downstream targets. Co-immunoprecipitation (Co-IP) confirmed specific interaction between Cx43 and c-Src proteins. Western blotting (WB) examined effects of Cx43 knockdown on expression of these predicted downstream targets. Finally, in vivo mouse xenografts validated Cx43's role in BC cell tumorigenesis. Cx43 was upregulated in bladder cancer tissues and its elevated expression correlated with poor patient prognosis. Silencing Cx43 significantly suppressed BC cell proliferation, migration, and invasion. Functional rescue experiments implicated the c-Src/PTEN pathway in mediating the oncogenic effects of Cx43. Mechanistically, Cx43 drives BC progression by facilitating c-Src-mediated suppression of the tumor suppressor PTEN and subsequent activation of FAK signaling. This study unveiled a novel regulatory pathway, Cx43 promotes malignant bladder cancer progression by modulating the c-Src/PTEN/p-FAK axis.
Indexed as
Identifiers
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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 Socratic graph.