Tumor-derived exosomal KPNA2 activates fibroblasts and interacts with KIFC1 to promote bladder cancer progression, a process inhibited by miR-26b-5p
Quick Facts
- Publication title: Tumor-derived exosomal KPNA2 activates fibroblasts and interacts with KIFC1 to promote bladder cancer progression, a process inhibited by miR-26b-5p
- Journal: Cell Mol Biol Lett
- Year: 2025
- DOI: 10.1186/s11658-025-00687-w
- PMID/PMCID: 39956902; PMC11830183
Research overview
To investigate the regulatory role of KPNA2 in BCa, we employed a comprehensive approach integrating clinical case data and bioinformatics analysis to evaluate the expression of KPNA2 in BCa tissues. These findings suggest that KPNA2 is a key gene that promotes BCa progression, can potentially be a novel tumor marker, and may serve as a new therapeutic target for BCa.
Key findings
Our research reveals that miR-26b-5p acts as an anticancer factor by targeting and inhibiting KPNA2 expression.
Furthermore, we have observed that the interaction between KPNA2 and Kinesin Family Member C1 (KIFC1) facilitates the transition of BCa cells into the G2/M phase, thereby promoting tumor advancement via activation of the Phosphoinositide 3-kinase (PI3K)- Protein Kinase B (AKT) pathway.
Importantly, this investigation is the first to identify KPNA2 expression in exosomes originating from BCa tissues.
Plasma exosomes from patients with BCa exhibited notably increased levels of KPNA2 compared with healthy controls, suggesting KPNA2 as a potential new tumor indicator.
Study design
To investigate the regulatory role of KPNA2 in BCa, we employed a comprehensive approach integrating clinical case data and bioinformatics analysis to evaluate the expression of KPNA2 in BCa tissues.
Mechanisms promoting cancer by KPNA2 were examined using both in vivo and in vitro models.
Echo Biotech Role
Echo Biotech contributed EV proteomics.
Related platforms: Exoomics®
Related services and capabilities: EV Proteomics
References
Original publication: Tumor-derived exosomal KPNA2 activates fibroblasts and interacts with KIFC1 to promote bladder cancer progression, a process inhibited by miR-26b-5p Cellular & molecular biology letters. 2025. DOI: 10.1186/s11658-025-00687-w. PMID/PMCID: 39956902; PMC11830183.