Role of STAT3/5 and Bcl-2/xL in 2-methoxyestradiol-induced endoreduplication of nasopharyngeal carcinoma cells

2011 ◽  
Vol 51 (12) ◽  
pp. 963-972 ◽  
Author(s):  
C.M. Ting ◽  
Chris K.C. Wong ◽  
R.N.S. Wong ◽  
K.W. Lo ◽  
Anne W.M. Lee ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cells

scholarly journals Anti-apoptotic role of TWIST and its association with Akt pathway in mediating taxol resistance in nasopharyngeal carcinoma cells

2007 ◽  
Vol 120 (9) ◽  
pp. 1891-1898 ◽  
Author(s):  
Xiaomeng Zhang ◽  
Qi Wang ◽  
Ming-Tat Ling ◽  
Yong Chuan Wong ◽  
Steve C.L. Leung ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cells ◽  
Akt Pathway ◽  
Taxol Resistance

scholarly journals ZNRF3 Inhibits the Invasion and Tumorigenesis in Nasopharyngeal Carcinoma Cells by Inactivating the Wnt/β-Catenin Pathway

2017 ◽  
Vol 25 (4) ◽  
pp. 571-577 ◽  
Author(s):  
Zhongwei Wang ◽  
Yali Wang ◽  
Hongtao Ren ◽  
Yingying Jin ◽  
Ya Guo
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Ring Finger ◽  
Carcinoma Cells ◽  
Tumor Xenograft ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
And Function

Zinc and ring finger 3 (ZNRF3), which belongs to the E3 ubiquitin ligase family, is involved in the progression and development of cancer. However, the expression and function of ZNRF3 in human nasopharyngeal carcinoma (NPC) remain unclear. Thus, the aim of this study was to investigate the role of ZNRF3 in human NPC. Our results showed that ZNRF3 was downregulated in NPC cell lines. Restoration of ZNRF3 significantly inhibited the proliferation of NPC cells and tumor xenograft growth in vivo. In addition, overexpression of ZNRF3 suppressed migration and invasion, as well as attenuated the epithelial‐mesenchymal transition (EMT) process in NPC cells. Furthermore, restoration of ZNRF3 obviously downregulated the expression levels of β-catenin, cyclin D1, and c-Myc in NPC cells. In conclusion, these data suggest that ZNRF3 inhibited the metastasis and tumorigenesis via suppressing the Wnt/β-catenin signaling pathway in NPC cells. Thus, ZNRF3 may act as a novel molecular target for the treatment of NPC.

Role of p38 MAPKs in Hypericin Photodynamic Therapy-induced Apoptosis of Nasopharyngeal Carcinoma Cells

2009 ◽  
Vol 85 (5) ◽  
pp. 1207-1217 ◽  
Author(s):  
Pui S. Chan ◽  
Ho K. Koon ◽  
Zhen G. Wu ◽  
Ricky N. S. Wong ◽  
Maria L. Lung ◽  
...  
Keyword(s):  
Photodynamic Therapy ◽  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cells ◽  
Induced Apoptosis ◽  
P38 Mapks

Transcription factor STAT1 promotes the proliferation, migration and invasion of nasopharyngeal carcinoma cells by upregulating LINC01160

2020 ◽  
Author(s):  
Jingang Ai ◽  
Guolin Tan ◽  
Tiansheng Wang ◽  
Wei Li ◽  
Ru Gao ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Nasopharyngeal Carcinoma ◽  
Chromatin Immunoprecipitation ◽  
Malignant Cell ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Cell Phenotype

Aim: To investigate the role of LINC01160 in nasopharyngeal carcinoma (NPC). Materials & methods: Using NPC cells CNE-2 and HNE-2 in vitro, we performed quantitative PCR to determine mRNA expression and western blotting to determine protein expression. CCK-8, transwell, flow cytometry and wound healing assays were done to examine the function of LINC01160 and STAT1. Chromatin immunoprecipitation PCR (ChIP-PCR) confirmed that STAT1 combines with the LINC01160 promoter region. Xenograft experiments were used to verify the role of STAT1 and LINC01160 in vivo. Results: LINC01160 is upregulated in NPC and can promote a malignant cell phenotype. STAT1 is a transcription factor of LINC01160 and can promote a malignant cell phenotype through upregulating LINC01160 expression. Conclusion: STAT1 can promote a malignant cell phenotype by upregulating LINC01160.

scholarly journals Human Caspase 12 Enhances NF-κB Activity through Activation of IKK in Nasopharyngeal Carcinoma Cells

2021 ◽  
Vol 22 (9) ◽  
pp. 4610
Author(s):  
Shu-Er Chow ◽  
Huei-Tzu Chien ◽  
Wing-Keung Chu ◽  
Victor Lin ◽  
Tzu-Hsiu Shen ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Ectopic Expression ◽  
Carcinoma Cells ◽  
Physical Interaction ◽  
Transfected Cells ◽  
Cellular Invasion ◽  
Caspase 12 ◽  
Catalytic Motif ◽  
Human Caspase

Human nasopharyngeal carcinoma (NPC) is a highly invasive cancer associated with proinflammation. Caspase-12 (Casp12), an inflammatory caspase, is implicated in the regulation of NF-κB-mediated cellular invasion via the modulation of the IκBα protein in NPC cells. However, the effect mechanisms of Casp12 need to be elucidated. NPC cells were transfected with the full length of human Casp12 cDNA (pC12) and the effect of human Casp12 (hCasp12) on the NF-κB activity was investigated. We found ectopic expression of hCasp12 increased the NF-κB activity accompanied by an increased p-IκBα expression and a decreased IκBα expression. Treatment of BMS, a specific IKK inhibitor, and pC12-transfected cells markedly decreased the NF-κB activity and ameliorated the expression level of IκBα reduced by hCasp12. Co-immunoprecipitation assays validated the physical interaction of hCasp12 with IKKα/β, but not with NEMO. Furthermore, the NF-κB activity of ΔCasp12-Q (a mutated catalytic of hCasp12) transfected cells was concentration-dependently induced, but lower than that of hCasp12-transfected cells. Importantly, the hCasp12-mediated NF-kB activity was enhanced by TNFα stimulation. That indicated a role of the catalytic motif of hCasp12 in the regulation of the NF-κB activity. This study indicated hCasp12 activated the NF-κB pathway through the activation of IKK in human NPC cells.

S100A14 Induces Apoptosis and Negatively Regulates Proliferation of Nasopharyngeal Carcinoma Cells

2021 ◽  
Author(s):  
Yu Xiao ◽  
Jibo Han ◽  
Fen Li ◽  
Anyuan Zheng ◽  
Qibing Chen ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Caspase 3 ◽  
Suppressor Gene ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Control Group ◽  
Phase Arrest ◽  
M Phase ◽  
Density Values

Abstract Background: S100A14 is involved in multiple pathological processes; however, its role in nasopharyngeal carcinoma is poorly understood. Methods: S100A14 was deleted or upregulated in 6-10B cells. Results: S100A14-knockdown 6-10B cells showed significantly higher optical density values in the CCK-8 assay, smaller scratch width in the scratch experiment, and significantly more invading cells in the transwell assay compared with controls. Compared with the control group, the G2/M and S phase proportions of the S100A14-overexpression group were significantly higher, early apoptosis was observed via JC-1 fluorescence, and flow cytometry showed a significantly higher proportion of apoptotic cells. Protein expression of Bcl-2 and Bcl-xl decreased significantly, whereas that of Bax, Bad, cleaved-PARP, and cleaved-caspase-3/9 increased. Conclusions: Knockdown of S100A14 promoted proliferation, migration, and invasion of 6-10B cells, whereas its upregulation promoted caspase-dependent apoptosis and induced S and G2/M phase arrest, indicating a role of S100A14 as a tumor suppressor gene in nasopharyngeal carcinoma.

scholarly journals ResolvinD1 attenuates high-mobility group box 1-induced epithelial-to-mesenchymal transition in nasopharyngeal carcinoma cells

2019 ◽  
Vol 244 (18) ◽  
pp. 1608-1618
Author(s):  
Pingli Yang ◽  
Shan Chen ◽  
Gang Zhong ◽  
Yan Wang ◽  
Weijia Kong ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Gene Silencing ◽  
Epithelial To Mesenchymal Transition ◽  
High Mobility ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
Emt Markers

Epithelial-to-mesenchymal transition (EMT) process is prevalent during the progression of tumors. Nasopharyngeal carcinoma (NPC) is no exception. High-mobility group box 1 (HMGB1) was reported to have the effect of inducing EMT in malignancy. However, the impact of HMGB1-induced EMT in NPC is unclear. Resolvin D1 (RvD1) was reported to regress the progression of inflammation and apoptosis of phagocytes. The effect of RvD1 in the EMT is largely unknown. The current research explored the role of RvD1 on HMGB1-induced EMT in NPC. EMT markers were investigated in 10 NPC and 10 nasopharyngitis (NPG) patients using immunohistochemistry and Western blot. In vitro, expression of EMT markers and HMGB1 in CNE1 and CNE2 cells was assessed with immunohistochemical, Western blot, and confocal microscopy after treatment with recombinant human HMGB1 (rhHMGB1) or HMGB1 gene silencing or RvD1. The invasion and migration of NPC cells were detected by scratch test and transwell assay. Overexpression and gene silencing of lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2) and G protein-coupled receptor 32 (GPR32) in CNE2 cells confirmed the effect of RvD1 using Western blots. N-cadherin, vimentin, and HMGB1 were found up-regulated in NPC samples compared with NPG samples, while ZO-1 and E-cadherin were down-regulated in NPC tissues. RhHMGB1-induced EMT in CNE1 and CNE2 cells in a dose-dependent way. CNE2 cell lines treated with rhHMGB1 possessed greater invasion and migration ability, which was confirmed by gene silencing. RvD1 suppressed HMGB1-induced EMT in NPC cells via ALX/FPR2 and GPR32 receptors. These results showed that EMT was obvious in NPC. HMGB1 played a key role in inducing EMT. RvD1 inhibited HMGB1-induced EMT and might have potential application in the area of NPC treatment. Impact statement Nasopharyngeal carcinoma has a high incidence in China. Discussing the molecular mechanism of nasopharyngeal carcinoma is important because of high recurrent rate and low quality of life after treatment. HMGB1, as an important inflammatory factor, promotes the process in many cancers. But little is known about how HMGB1 affects the progress of nasopharyngeal carcinoma cells. In our research, we assessed the role of HMGB1 on metastasis and invasion of nasopharyngeal carcinoma cells. The result of study indicates HMGB1-induced EMT in nasopharyngeal carcinoma cells. Furthermore, we observed that RvD1, which plays an actively protective role in many diseases, controls the migration and invasion of nasopharyngeal carcinoma cells by inhibiting the HMGB1-induced EMT. RvD1 can be further studied as a protective factor for nasopharyngeal carcinoma.

scholarly journals Up-regulation of miR-34c-5p inhibits nasopharyngeal carcinoma cells by mediating NOTCH1

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Xin Xu ◽  
Haomin Yan ◽  
Le Zhang ◽  
Jing Liu ◽  
Yu Huang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Biological Function ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Normal Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Rescue Experiment ◽  
And Migration

Abstract Objective: To explore the correlation between miR-34c-5p and NOTCH1 in nasopharyngeal carcinoma (NPC). Materials and methods: qPCR was employed to quantify miR-34c-5p and NOTCH1 mRNA in NPC, and Western blot to detect NOTCH1. MiR-34c-5p mimics/inhibitor and NOTCH1 siRNA were constructed to analyze the role of miR-34c-5p/NOTCH1 on the biological function of NPC cells. Results: NPC cells showed lower miR-34c-5p expression and higher NOTCH1 expression than normal cells, and up-regulating miR-34c-5p or inhibiting NOTCH1 could strongly suppress the epithelial–mesenchymal transition (EMT), proliferation, invasion and migration of NPC cells, and induce apoptosis in them. Up-regulating miR-34c-5p could inhibit NOTCH1, and miR-34c-5p was negatively correlated with NOTCH1. Rescue experiment results revealed that NOTCH1 up-regulation could counteract the changes of cell process induced by increased miR-34c-5p. Conclusion: MiR-34c-5p inhibits the growth of NPC by down-regulating NOTCH1, so up-regulating miR-34c-5p or down-regulating NOTCH1 may become the potential direction of NPC treatment.

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