肿瘤来源的外泌体KPNA2激活成纤维细胞并与KIFC1相互作用以促进膀胱癌症进展，这一过程被miR-26b-5p抑制

核心信息

  • 论文英文标题: Tumor-derived exosomal KPNA2 activates fibroblasts and interacts with KIFC1 to promote bladder cancer progression, a process inhibited by miR-26b-5p
  • 期刊: Cell Mol Biol Lett
  • 发表年份: 2025
  • DOI: 10.1186/s11658-025-00687-w
  • PMID/PMCID: 39956902; PMC11830183

研究概览

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.

核心发现

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.

研究设计

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 角色

膀胱癌和癌旁组织外泌体4D LFQ蛋白质组

关联平台: Exoomics®

关联服务与能力: EV Proteomics

关联产品或试剂: 无明确产品引用

参考文献

原始论文: 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.