2015
DOI: 10.1038/onc.2015.402
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EB-virus latent membrane protein 1 potentiates the stemness of nasopharyngeal carcinoma via preferential activation of PI3K/AKT pathway by a positive feedback loop

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, LMP… Show more

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Cited by 60 publications
(40 citation statements)
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“…LMP1 is widely acknowledged to act as an important oncoprotein that modulates several signaling pathways, including the nuclear factor kappa B (NF-κB), c-Jun N-terminal kinase (JNK), and phosphatidylinositol 3-kinase(PI3K) signaling pathways, thus promoting cell growth and suppressing apoptosis [31, 32]. In NPC for example, LMP1 preserves the cancer stemness of NPC cells by activating the PI3K/AKT pathway [33]; LMP1 critically mediates transformation of nasopharyngeal epithelial cells and facilitates FGF2/FGFR1 signaling activation in the EBV-driven pathogenesis of NPC [34]. In lymphoma, LMP1 protects lymphoma cells from cell death through the collagen-mediated activation of a receptor tyrosine kinase and makes an important contribution to promote the oncogenic effects of EBV [35]; LMP1 has also been reported to aggravate malignant cell function, induce surviving expression and inhibit cell apoptosis through NF-κB and PI3K/Akt signaling pathways [9, 36].…”
Section: Discussionmentioning
confidence: 99%
“…LMP1 is widely acknowledged to act as an important oncoprotein that modulates several signaling pathways, including the nuclear factor kappa B (NF-κB), c-Jun N-terminal kinase (JNK), and phosphatidylinositol 3-kinase(PI3K) signaling pathways, thus promoting cell growth and suppressing apoptosis [31, 32]. In NPC for example, LMP1 preserves the cancer stemness of NPC cells by activating the PI3K/AKT pathway [33]; LMP1 critically mediates transformation of nasopharyngeal epithelial cells and facilitates FGF2/FGFR1 signaling activation in the EBV-driven pathogenesis of NPC [34]. In lymphoma, LMP1 protects lymphoma cells from cell death through the collagen-mediated activation of a receptor tyrosine kinase and makes an important contribution to promote the oncogenic effects of EBV [35]; LMP1 has also been reported to aggravate malignant cell function, induce surviving expression and inhibit cell apoptosis through NF-κB and PI3K/Akt signaling pathways [9, 36].…”
Section: Discussionmentioning
confidence: 99%
“…In NPC, phosphorylation of Akt is frequently observed and is related to the malignant phenotype [3638]. EBV encodes latent membrane protein 1 (LMP1), which contributes to loss of function of PTEN, an inhibitor of the PI3K/Akt pathway, by upregulating miR-21, thus potentiating NPC [39] and promoting chemoresistance [40]. In addition, LMP1 stimulates anaerobic glycolysis by activating Akt [30].…”
Section: Discussionmentioning
confidence: 99%
“…LMP1, PI3K/AKT, miR-21 and PTEN could constitute a positive feedback loop that regulates LMP1-induced CSCs in NPC cell. [36]Some sequence variations of LMP1 may lead to a potential escape from host cell immune recognition, protecting latent EBV infection and causing an increase in tumorigenicity [37]. …”
Section: Lmp1mentioning
confidence: 99%