ArticleOncogene2016
EB-virus latent membrane protein 1 potentiates the stemness of nasopharyngeal carcinoma via preferential activation of PI3K/AKT pathway by a positive feedback loop.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 83 citations in OpenAlex.
- Rapamycin Targets Cancer Stem Cells to Decrease Cisplatin Resistance in a Head and Neck Cancer Mouse Xenograft Model.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026Article
- Chelerythrine: a novel candidate for targeting miR-21/PTEN/PI3K/AKT in nasopharyngeal carcinoma.Journal of translational medicine · 2026Article
- CD44 expression associates with EBV LMP1, reduced CD8⁺ T cell infiltration, and lower PD-L1 combined positive score in nasopharyngeal carcinoma.Infectious agents and cancer · 2026Article
- Active Components and Potential Mechanism of Redujing Oral Liquid for Treating EBV Infection: A UHPLC-MS and Network Pharmacology- Based Approach.Combinatorial chemistry & high throughput screening · 2026Article
- Artificial Intelligence-Enabled Multi-Omics for Predicting Immune Checkpoint Inhibitor Response and Resistance.Journal of multidisciplinary healthcare · 2026Review
- SOX4-ZIP14-zinc metabolism mediates oncogenesis and suppresses T cell immunity in nasopharyngeal carcinoma.Cell reports. Medicine · 2025Article
- Oncoviruses in the Oral Cavity: Recent Advances in Understanding Viral Infections and Tumorigenesis.International journal of molecular sciences · 2025Review
- Epstein-Barr virus-infected nasopharyngeal carcinoma therapeutics: oncoprotein targets and clinical implications.Medical oncology (Northwood, London, England) · 2025Review
- Review
- Article
- Feedback loop between hypoxia and energy metabolic reprogramming aggravates the radioresistance of cancer cells.Experimental hematology & oncology · 2024Review
- Environmental pollutants and phosphoinositide signaling in autoimmunity.Journal of hazardous materials · 2024Review
- Epstein-Barr Virus Promotes Oral Squamous Cell Carcinoma Stemness through the Warburg Effect.International journal of molecular sciences · 2023Article
- The Role of Exosomes in Epithelial-to-Mesenchymal Transition and Cell Functional Properties in Head and Neck Cancer.Cancers · 2023Review
- Protein Kinase CK2 and Epstein-Barr Virus.Biomedicines · 2023Review
- Targeted therapy for head and neck cancer: signaling pathways and clinical studies.Signal transduction and targeted therapy · 2023Review
- MiRNA signatures in nasopharyngeal carcinoma: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2023Review
- Signaling pathways in the regulation of cancer stem cells and associated targeted therapy.MedComm · 2022Review
- Improving on-treatment risk stratification of cancer patients with refined response classification and integration of circulating tumor DNA kinetics.BMC medicine · 2022Article
- The Role of hsa-miR-21 and Its Target Genes Involved in Nasopharyngeal Carcinoma.Asian Pacific journal of cancer prevention : APJCP · 2021Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous study reported that Epstein-Barr virus(EBV)-encoded latent membrane protein 1 (LMP1) could induce development of CD44(+/High) stem-like cells in nasopharyngeal carcinoma (NPC). However, the molecular mechanisms that underlie modulation of cancer stem cells (CSCs) in NPC remain unclear. Here, we show that LMP1 induced CSC-like properties through promotion of the expression of epithelial-mesenchymal transition-like cellular markers and through alterations in differentiation markers. Furthermore, LMP1 activated and triggered phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway, which subsequently stimulated expression of CSC markers, development of side population and tumor sphere formation. This suggests that PI3K/AKT pathway has an important role in the induction and maintenance of CSC properties in NPC. Similarly, PI3K/AKT pathway was also activated by phosphorylase in LMP1-induced CD44(+/High) cells. In addition, LMP1 greatly increased expression of miR-21 and downregulated expression of the miR-21 target, PTEN. Overexpression of miR-21 by transfection of miR-21 mimics into LMP1-transformed cells led to phosphorylase-mediated activation of the PI3K/AKT pathway and induction of CSCs. On the contrary, phosphorylation of the PI3K/AKT pathway and the expression of CSC were reversed by an miR-21 inhibitor. The specific inhibitor (Ly294002) of PI3K/AKT pathway significantly decreased expression of miR-21 and CSC markers and upregulated the expression of PTEN, which indicates that miR-21 and PTEN are the downstream effectors of PI3K/AKT and that expression of these two effectors are related to the development of NPC CSCs. Taken together, our novel findings indicate that LMP1, PI3K/AKT, miR-21 and PTEN constitute a positive feedback loop and have a key role in LMP1-induced CSCs in NPC.
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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.