ArticleBritish journal of cancer2023
PTBP1 drives c-Myc-dependent gastric cancer progression and stemness.
Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- Regulation of Tau Alternative Splicing: A Novel Role for the Ribonucleoprotein RBM20.International journal of molecular sciences · 2026Article
- PTBP1 and Cancer: From RNA Regulation to Therapeutic Potential.Journal of cellular and molecular medicine · 2025Review
- Design, synthesis, and antitumor activity of novel thioheterocyclic nucleoside derivatives by suppressing the c-MYC pathway.Acta pharmaceutica Sinica. B · 2025Article
- Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025Review
- PTBP1 as a potential regulator of disease.Molecular and cellular biochemistry · 2024Review
- PTBP1 knockdown impairs autophagy flux and inhibits gastric cancer progression through TXNIP-mediated oxidative stress.Cellular & molecular biology letters · 2024Article
- Terpene extract from the stem ofJournal of pharmaceutical analysis · 2024Article
- Endoplasmic reticulum stress-induced senescence in human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Review
- RAVER1 hinders lethal EMT and modulates miR/RISC activity by the control of alternative splicing.Nucleic acids research · 2024Article
- Epigenetic silencing ofEpigenomics · 2024Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundGastric cancer (GC) tumorigenesis and treatment failure are caused by cancer stem cells. Polypyrimidine tract binding protein 1 (PTBP1) was shown to be involved in the development of embryonic stem cells and is now being considered as a therapeutic target for tumour progression and stem-cell characteristics.
methodsPTBP1 expression in GC samples was detected using tissue microarrays. Proliferation, colony formation, spheroid formation and stem-cell analysis were used to examine PTBP1's role in tumorigenesis and stem-cell maintenance. In AGS and HGC-27 cells with or without PTBP1 deficiency, ubiquitin-related protein expression and co-precipitation assays were performed.
resultsWe identified that PTBP1 was aberrantly highly expressed and represented a novel prognostic factor in GC patients. PTBP1 maintained the tumorigenic activity and stem-cell characteristics of GC in vitro and in vivo. PTBP1 directly interacts with c-Myc and stabilises its protein levels by preventing its proteasomal degradation. This is mediated by upregulating the ubiquitin-specific proteases USP28 and limiting FBW7-mediated ubiquitination of c-Myc. Moreover, the depletion of PTBP1-caused tumour regression was significantly compromised by exogenous c-Myc expression.
conclusionsBy preserving the stability of c-Myc through the ubiquitin-proteasome pathway, the oncogene PTBP1 supports stem-cell-like phenotypes of GC and is involved in GC progression.
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