ArticleCell death & disease2023
KIF15 is essential for USP10-mediated PGK1 deubiquitination during the glycolysis of pancreatic cancer.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 21 citations in OpenAlex.
- PGK1 epigenetically silences STING via DNMT1 and its knockdown synergizes with STING agonists in pancreatic cancer.Acta pharmacologica Sinica · 2026Article
- KIF15 (Kinesin-12): molecular biology, physiological functions, and roles in disease.Journal of cancer research and clinical oncology · 2026Review
- USP10 deubiquitinase: Physiological function, diseases and therapeutic target (Review).International journal of molecular medicine · 2026Review
- The YY1-KIF15-PRDX1 axis promotes gastric cancer progression by inducing mitochondrial ROS imbalance.Oncogene · 2026Article
- PARK2-Mediated PGK1 Degradation Suppresses Partial Epithelial-Mesenchymal Transition and Metastasis in Triple-Negative Breast Cancer.Oncology research · 2026Article
- Co-targeting MRPS7-23 synergistically enhances cisplatin efficacy to suppress nasopharyngeal carcinoma growth and metastasis.International journal of biological sciences · 2026Article
- Post-Translational Modifications: Key "Regulators" of Pancreatic Cancer Malignant Phenotype-Advances in Mechanisms and Targeted Therapies.Biomedicines · 2025Review
- The multifaceted roles of deubiquitinating enzymes (DUBs) in pancreatic ductal adenocarcinoma.Cell death & disease · 2025Review
- USP10 Inhibits Ferroptosis via Deubiquinating POLR2A in Head and Neck Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The multifaceted role of KIF15 in cancer progression and therapy.Investigational new drugs · 2025Review
- ALDOC and PGK1 coordinately induce glucose metabolism reprogramming and promote development of colorectal cancer.Molecular medicine (Cambridge, Mass.) · 2025Article
- Atractylenolide I ameliorated the growth and enzalutamide resistance of castration-resistant prostate cancer by targeting KIF15.Chinese medicine · 2025Article
- Lactylome analysis reveals potential target modified proteins in the retina of form-deprivation myopia.iScience · 2024Article
- Integrated machine learning algorithms identify KIF15 as a potential prognostic biomarker and correlated with stemness in triple-negative breast cancer.Scientific reports · 2024Article
- USP10 promotes pancreatic ductal adenocarcinoma progression by attenuating FOXC1 protein degradation to activate the WNT signaling pathway.International journal of biological sciences · 2024Article
- KIF15 promotes human glioblastoma progression under the synergistic transactivation of REST and P300.International journal of biological sciences · 2024Article
- USP10 promotes intrahepatic cholangiocarcinoma cell survival and stemness via SNAI1 deubiquitination.Journal of molecular histology · 2023Article
- BHLHE40, a potential immune therapy target, regulated by FGD5-AS1/miR-15a-5p in pancreatic cancer.Scientific reports · 2023Article
- Regulation of phosphoglycerate kinase 1 and its critical role in cancer.Cell communication and signaling : CCS · 2023Review
- Ubiquitin signaling in pancreatic ductal adenocarcinoma.Frontiers in molecular biosciences · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycolysis is the most predominant metabolic reprogramming of pancreatic cancer (PC), the underlying mechanism of which in PC cells remains unclear. In this study, we found for the first time that KIF15 promotes the glycolytic capacity of PC cells and PC tumor growth. Moreover, the expression of KIF15 was negatively correlated with the prognosis of PC patients. The ECAR and OCR measurements indicated that KIF15 knockdown significantly impaired the glycolytic capacity of PC cells. Western blotting demonstrated that the expression of glycolysis molecular markers decreased rapidly after the knockdown of KIF15. Further experiments revealed that KIF15 promoted the stability of PGK1 and its effect on PC cell glycolysis. Interestingly, the overexpression of KIF15 impaired the ubiquitination level of PGK1. To investigate the underlying mechanism by which KIF15 regulates the function of PGK1, we performed mass spectrometry (MS). The MS and Co-IP assay indicated that KIF15 recruited and enhanced the binding between PGK1 and USP10. The ubiquitination assay verified that KIF15 recruited and promoted the effect of USP10 on PGK1, thereby deubiquitinating PGK1. Through the construction of KIF15 truncators, we found that KIF15 is bound to PGK1 and USP10 through its coil2 domain. Together, our study demonstrated for the first time that KIF15 enhances the glycolytic capacity of PC through the recruitment of USP10 and PGK1, and that the KIF15/USP10/PGK1 axis may serve as an effective therapeutic agent for PC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.