ArticleCellular & molecular biology letters2024
PTBP1 knockdown impairs autophagy flux and inhibits gastric cancer progression through TXNIP-mediated oxidative stress.
Article in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Reprogramming of cell death in gastric cancer: From molecular mechanisms to therapeutic potential (Review).International journal of molecular medicine · 2026Review
- Exercise is associated with attenuated aging-related osteoporosis through TMAO alpha Klotho inflammasome signaling.iScience · 2026Article
- Role and Mechanism ofInternational journal of molecular sciences · 2026Article
- Article
- The PTBP1-EZH2-DOCK2 axis promotes M1 microglial polarization and exacerbates neuronal apoptosis following spinal cord injury.Journal of orthopaedic translation · 2026Article
- PTBP1 functions as a suppressor of ferroptosis in endometrial carcinoma cells by stabilizing SLC7A11 mRNA.Discover oncology · 2025Article
- Study of the mechanism of methyltransferase 3 regulation of ferroptosis in allergic rhinitis and promotion of allergic rhinitis in an m6A-dependent mechanism.Journal of inflammation (London, England) · 2025Article
- FNDC3B promotes gastric cancer metastasis via interacting with FAM83H and preventing its proteasomal degradation.Cellular & molecular biology letters · 2025Article
- Silencing hnRNPD inhibits gastric cancer growth by increasing TXNIP-mediated oxidative stress.Discover oncology · 2025Article
- Curcumin inhibits colorectal cancer progression by targeting PTBP1 and CDK2-mediated pathways.Frontiers in oncology · 2025Article
- Crucial roles of CircRNA-mediated autophagy in digestive cancer.Frontiers in oncology · 2025Review
- Multiomics integration and machine learning reveal prognostic programmed cell death signatures in gastric cancer.Scientific reports · 2024Article
- Hypoxia-driven M2-polarized macrophages facilitate the epithelial-mesenchymal transition of glioblastoma via extracellular vesicles.Theranostics · 2024Article
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17 authors.
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Abstract
backgroundGastric cancer (GC) is a prevalent malignant tumor, and the RNA-binding protein polypyrimidine tract-binding protein 1 (PTBP1) has been identified as a crucial factor in various tumor types. Moreover, abnormal autophagy levels have been shown to significantly impact tumorigenesis and progression. Despite this, the precise regulatory mechanism of PTBP1 in autophagy regulation in GC remains poorly understood.
methodsTo assess the expression of PTBP1 in GC, we employed a comprehensive approach utilizing western blot, real-time quantitative polymerase chain reaction (RT-qPCR), and bioinformatics analysis. To further identify the downstream target genes that bind to PTBP1 in GC cells, we utilized RNA immunoprecipitation coupled with sequencing (si-PTBP1 RNA-seq). To evaluate the impact of PTBP1 on gastric carcinogenesis, we conducted CCK-8 assays, colony formation assays, and GC xenograft mouse model assays. Additionally, we utilized a transmission electron microscope, immunofluorescence, flow cytometry, western blot, RT-qPCR, and GC xenograft mouse model experiments to elucidate the specific mechanism underlying PTBP1's regulation of autophagy in GC.
resultsOur findings indicated that PTBP1 was significantly overexpressed in GC tissues compared with adjacent normal tissues. Silencing PTBP1 resulted in abnormal accumulation of autophagosomes, thereby inhibiting GC cell viability both in vitro and in vivo. Mechanistically, interference with PTBP1 promoted the stability of thioredoxin-interacting protein (TXNIP) mRNA, leading to increased TXNIP-mediated oxidative stress. Consequently, this impaired lysosomal function, ultimately resulting in blockage of autophagic flux. Furthermore, our results suggested that interference with PTBP1 enhanced the antitumor effects of chloroquine, both in vitro and in vivo.
conclusionPTBP1 knockdown impairs GC progression by directly binding to TXNIP mRNA and promoting its expression. Based on these results, PTBP1 emerges as a promising therapeutic target for GC.
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