ArticleCancer science2023
LPLUNC1 reduces glycolysis in nasopharyngeal carcinoma cells through the PHB1-p53/c-Myc axis.
Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- LINC00312 increases gemcitabine sensitivity in nasopharyngeal carcinoma by recruiting PABPC1 and modulating PAX5-mediated transcription of LPLUNC1.NPJ precision oncology · 2026Article
- A review on the role of IL-6 in the onset and progression of nasopharyngeal carcinoma.Medical oncology (Northwood, London, England) · 2025Review
- S100A2 upregulates GLUT1 expression to promote glycolysis in the progression of nasopharyngeal carcinoma.Histology and histopathology · 2024Article
- ELAVL1 regulates glycolysis in nasopharyngeal carcinoma cells through the HMGB3/β-catenin axis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Prohibitin 1 inhibits cell proliferation and induces apoptosisWorld journal of gastrointestinal oncology · 2024Article
- Metabolic reprogramming in the pathogenesis and progression of nasopharyngeal carcinoma: molecular mechanisms and therapeutic implications.American journal of cancer research · 2024Review
- ARHGAP44-mediated regulation of the p53/C-myc/Cyclin D1 pathway in modulating the malignant biological behavior of osteosarcoma cells.Journal of orthopaedic surgery and research · 2023Article
- TOM40 regulates the progression of nasopharyngeal carcinoma through ROS-mediated AKT/mTOR and p53 signaling.Discover oncology · 2023Article
- LPLUNC1 reduces glycolysis in nasopharyngeal carcinoma cells through the PHB1-p53/c-Myc axis.Cancer science · 2023Article
Corrections and comments
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Authors and funding
19 authors at 1 institution in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells prefer glycolysis to support their proliferation. Our previous studies have shown that the long palate, lung, and nasal epithelial cell clone 1 (LPLUNC1) can upregulate prohibitin 1 (PHB1) expression to inhibit the proliferation of nasopharyngeal carcinoma (NPC) cells. Given that PHB1 is an important regulator of cell energy metabolism, we explored whether and how LPLUNC1 regulated glucose glycolysis in NPC cells. LPLUNC1 or PHB1 overexpression decreased glycolysis and increased oxidative phosphorylation (OXPHOS)-related protein expression in NPC cells, promoting phosphorylated PHB1 nuclear translocation through 14-3-3σ. LPLUNC1 overexpression also increased p53 but decreased c-Myc expression in NPC cells, which were crucial for the decrease in glycolysis and increase in OXPHOS-related protein expression induced by LPLUNC1 overexpression. Finally, we found that treatment with all-trans retinoic acid (ATRA) reduced the viability and clonogenicity of NPC cells, decreased glycolysis, and increased OXPHOS-related protein expression by enhancing LPLUNC1 expression in NPC cells. Therefore, the LPLUNC1-PHB1-p53/c-Myc axis decreased glycolysis in NPC cells, and ATRA upregulated LPLUNC1 expression, ATRA maybe a promising drug for the treatment of NPC.
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