Oncogenic <scp>S1P</scp> signalling in <scp>EBV</scp>‐associated nasopharyngeal carcinoma activates <scp>AKT</scp> and promotes cell migration through <scp>S1P</scp> receptor 3

Lee, Hui Min; Lo, Kwok Wai; Wei, Wenbin; Tsao, Sai Wah; Chung, Grace; Ibrahim, Maha; Dawson, Christopher W.; Murray, Paul G.; Paterson, Ian C.; Yap, Lee Fah

doi:10.1002/path.4879

Cited by 38 publications

(28 citation statements)

References 39 publications

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“…For instance, besides S1PR 1-3 , the roles of other S1PRs in angiogenic factor secretion need further investigation. Moreover, S1P has been shown to promote the activation of several intracellular signal transduction cascades, including NF-κB signaling [ 27 ], ERK1/2 signaling [ 28 ] and Akt signaling [ 29 ]. Further studies need to be carried out to determine the signaling pathway through which S1P induced the angiogenic factor secretion.…”

Section: Discussionmentioning

confidence: 99%

Sphingosine kinase 1/sphingosine-1-phosphate (S1P)/S1P receptor axis is involved in ovarian cancer angiogenesis

et al. 2017

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Sphingosine kinase (SphK)/sphingosine-1-phosphate (S1P)/S1P receptor (S1PR) signaling pathway has been implicated in a variety of pathological processes of ovarian cancer. However, the function of this axis in ovarian cancer angiogenesis remains incompletely defined. Here we provided the first evidence that SphK1/S1P/S1PR1/3 pathway played key roles in ovarian cancer angiogenesis. The expression level of SphK1, but not SphK2, was closely correlated with the microvascular density (MVD) of ovarian cancer tissue. In vitro, the angiogenic potential and angiogenic factor secretion of ovarian cancer cells could be attenuated by SphK1, but not SphK2, blockage and were restored by the addition of S1P. Moreover, in these cells, we found S1P stimulation induced the angiogenic factor secretion via S1PR1 and S1PR3, but not S1PR2. Furthermore, inhibition of S1PR1/3, but not S1PR2, attenuated the angiogenic potential and angiogenic factor secretion of the cells. in vivo, blockage of SphK or S1PR1/3 could attenuate ovarian cancer angiogenesis and inhibit angiogenic factor expression in mouse models. Collectively, the current study showed a novel role of SphK1/S1P/S1PR1/3 axis within the ovarian cancer, suggesting a new target to block ovarian cancer angiogenesis.

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Section: Discussionmentioning

confidence: 99%

Sphingosine kinase 1/sphingosine-1-phosphate (S1P)/S1P receptor axis is involved in ovarian cancer angiogenesis

et al. 2017

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“…Overexpression of SphK facilitates cancer development [45,50]. S1P signaling in Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma activates protein kinase B (Akt, PKB) and promotes cell migration through S1P receptor 3 (S1PR3), while a knockdown of S1PR3 decreases Akt activation and the S1P-triggered migration of nasopharyngeal carcinoma cells in vitro [51].…”

Section: Pathogenic Stimulusmentioning

confidence: 99%

Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

Brücher

Jamall

2019

4open

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A pathogenic (biological or chemical) stimulus is the earliest information received by a cell that can result in the disruption of homeostasis with consequent development of disease. Chronic inflammation involves many cell types with numerous cytokines and signaling pathways, the release of different components by the cells, and the crosstalk provoked by such stimuli involving subclinical chronic inflammation and is mechanistically manifold. Exosomes secrete chemicals that trigger the epithelium to produce exosome-like nanoparticles promoting chronic inflammation. Small molecules, together with various cytokines, selectively target signaling pathways inducing crosstalk that suppress apoptosis. 16S rRNA gene sequencing has become routine to provide information on the composition and abundance of bacteria found in human tissues and in reservoirs. The deregulation of autophagy with chronic stimulation of inflammation is an early phenomenon in carcinogenesis. The disruption of cell–cell integrity enables transcellular CagA migration and triggers deregulation of autophagy with the net result being chronic inflammation. The complex and insidious nature of chronic inflammation can be seen both inside and outside the cell and even with intracellular nuclear fragments such as chromatin, which itself can elicit a chronic inflammatory response within the cytoplasm and affect autophagy. The ultimate result of unresolved chronic inflammation is fibrosis, a step before tissue remodeling results in the formation of a precancerous niche (PCN). Various pathogenic stimuli associated with different neoplasms result in persistent inflammation. This ongoing disruption of homeostasis in the micromilieu of cells, tissues, and organs is an essential preamble to carcinogenesis and occurs early in that process.

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“…Elderly people above the age group of 65 years are more susceptible to NPC‐related mortality, and the incidence rate is much higher in China with 40.14% 3,4 . Epstein‐Barr virus Infection considered being the one of the major risk factors of NPC, whereas it is also reported to cause due to the environment factors, 5 tobacco smoking, 6 and genetic predisposition 7 . The overall 5‐year survival rate of NPC patients was decreased from 100% to 86.1% due to their poor prognosis 8 .…”

Section: Introductionmentioning

confidence: 99%

Fucoxanthin treatment inhibits nasopharyngeal carcinoma cell proliferation through induction of autophagy mechanism

Long

Cao

Zhao³

et al. 2020

Environmental Toxicology

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Nasopharyngeal carcinoma (NPC) arises from the epithelium of the nasopharyngeal mucosa. Elderly people above the age of 65 years are more susceptible to NPC. Nasopharyngectomy is the renowned treatment procedure to NPC; however, it is too risky due to its complicated surgical procedure. Other treatment methods also reported with serious side effects such brain injury; hence, the alternative anticancer drug without any side effects was needed. Fucoxanthin is a carotenoid derived from marine algae with the numerous pharmacological functions. This study aims to examine the inhibitory potential in NPC cell proliferation via apoptosis and autophagy. The cytotoxicity of fucoxanthin on C666‐1 cells was observed by the MTT assay. The expression of autophagy‐linked proteins was assessed with immunoblotting analysis. The expression of autophagy protein LC3 was estimated using immunocytochemical analysis in C666‐1 and GFP‐LC3 transfected cells. Furthermore, the fucoxanthin‐treated C666‐1 cells were analyzed with TUNEL assay. The apoptotic level in the fucoxanthin‐treated C666‐1 cells was evaluated using acridine orange staining. Fucoxanthin significantly increased the expression of autophagy‐linked proteins which is clearly depicted in the immunoblotting analysis and immunocytochemical analysis of GFP‐tagged LC3 protein. The results of TUNEL assay of fucoxanthin‐treated C666‐1 in the presence autophagy inhibitors demonstrated the induction of autophagy by fucoxanthin. Acridine orange staining results of C666‐1 confirmed fucoxanthin decreases the expression of autophagy‐linked proteins during stressed condition thereby causes apoptosis. Our overall results authentically conclude that fucoxanthin induces autophagy and apoptosis in NPC cell line, and it can be ideal agent to treat nasopharyngeal cancer in future with further investigations.

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Oncogenic S1P signalling in EBV‐associated nasopharyngeal carcinoma activates AKT and promotes cell migration through S1P receptor 3

Cited by 38 publications

References 39 publications

Sphingosine kinase 1/sphingosine-1-phosphate (S1P)/S1P receptor axis is involved in ovarian cancer angiogenesis

Sphingosine kinase 1/sphingosine-1-phosphate (S1P)/S1P receptor axis is involved in ovarian cancer angiogenesis

Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

Fucoxanthin treatment inhibits nasopharyngeal carcinoma cell proliferation through induction of autophagy mechanism

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