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.

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
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