Gastric cancer (GC) is a leading cause of cancer-related deaths worldwide. Poly(rC) binding protein 2 (PCBP2), an RNA binding protein, has been reported to be involved in the progression of various cancers. However, the role of PCBP2 in GC and its underlying mechanisms remain elusive. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect mRNA expression, whereas western blotting and immunohistochemistry assays were used to detect protein expression levels. Cell proliferation, migration, and invasion were assessed by EdU assay, wound-healing assay, and transwell assay, respectively. The levels of reactive oxygen species (ROS), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and iron (Fe²⁺) were detected using commercial assay kits. RIP assay was conducted to analyze the relationship between PCBP2 and trophinin-associated protein (TROAP). Actinomycin D assay was performed to investigate the effect of PCBP2 depletion on TROAP mRNA stabilization. Finally, a subcutaneous xenograft mouse model was established to validate the effect of PCBP2 depletion on tumor formation. PCBP2 expression was upregulated in GC tissues and cells, and its depletion inhibited GC cell proliferation, migration, and invasion. Additionally, PCBP2 depletion promoted ferroptosis, a novel form of cell death mediated by iron. TROAP expression was also upregulated in GC tissues and cells, and PCBP2 stabilized TROAP mRNA expression in GC cells. Knocking down PCBP2 regulated GC cell proliferation, migration, invasion, and ferroptosis by reducing TROAP expression. Furthermore, PCBP2 knockdown repressed aggressive behavior of GC cells in vivo. Our study demonstrated that PCBP2 stabilized TROAP to promote the malignant progression of gastric cancer. Targeting PCBP2 and its downstream target TROAP may provide a novel therapeutic strategy for the treatment of gastric cancer.

01 Feb 2025·Mucosal Immunology

Corrigendum to “Stress systems exacerbate the inflammatory response after corneal abrasion in sleep-deprived mice via the IL-17 signaling pathway” [Mucosal Immunol. 17(3) (2024) 323–345]

Author: Yan, Ruyu ; Liu, Jun ; Li, Yan ; Xue, Yunxia ; Liu, Sijing ; Hu, Yu ; Liu, Shutong ; Xu, Pengyang ; Fu, Ting ; Li, Zhijie

01 Oct 2024·Experimental Cell Research

miRNA-193a-mediated WT1 suppression triggers podocyte injury through activation of the EZH2/β-catenin/NLRP3 pathway in children with diabetic nephropathy

Article

Author: Yang, Jing ; Wang, Yingying ; Gao, Yang ; Qi, Ying ; Gao, Pinli ; Zhao, Xiaowei ; Liu, Juan ; Wang, Peng ; Dai, Shasha

Diabetic nephropathy (DN), an eminent etiology of renal disease in patients with diabetes, involves intricate molecular mechanisms. Recent investigations have elucidated microRNA-193a (miR-193a) as a pivotal modulator in DN, although its precise function in podocyte impairment remains obscure. The present study investigated the role of miR-193a in podocyte injury via the WT1/EZH2/β-catenin/NLRP3 pathway. This study employed a comprehensive experimental approach involving both in vitro and in vivo analyses. We utilized human podocyte cell lines and renal biopsy samples from pediatric patients with DN. The miR-193a expression levels in podocytes and glomeruli were quantified via qRT‒PCR. Western blotting and immunofluorescence were used to assess the expression of WT1, EZH2, β-catenin, and NLRP3 inflammasome components. Additionally, the study used luciferase reporter assays to confirm the interaction between miR-193a and WT1. The impact of miR-193a manipulation was observed by overexpressing WT1 and inhibiting miR-193a in podocytes, followed by analysis of downstream pathway activation and inflammatory markers. We found upregulated miR-193a in podocytes and glomeruli, which directly targeted and suppressed WT1, a crucial podocyte transcription factor. WT1 suppression, in turn, activated the EZH2/β-catenin/NLRP3 pathway, leading to inflammasome assembly and proinflammatory cytokine production. Overexpression of WT1 or inhibition of miR-193a attenuated these effects, protecting podocytes from injury. This study identified a novel mechanism by which miR-193a-mediated WT1 suppression triggers podocyte injury in DN via the EZH2/β-catenin/NLRP3 pathway. Targeting this pathway or inhibiting miR-193a may be potential therapeutic strategies for DN.

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