Increase in IkappaB kinase alpha expression suppresses the tumor progression and improves the prognosis for nasopharyngeal carcinoma

2013 ◽  
Vol 54 (2) ◽  
pp. 156-165 ◽  
Author(s):  
Ling Deng ◽  
Yan Li ◽  
Ping Ai ◽  
Yuxin Xie ◽  
Hong Zhu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Progression ◽  
Ikappab Kinase

scholarly journals Serum CXCL9 Levels Are Associated with Tumor Progression and Treatment Outcome in Patients with Nasopharyngeal Carcinoma

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e80052 ◽  
Author(s):  
Li-Jen Hsin ◽  
Huang-Kai Kao ◽  
I-How Chen ◽  
Ngan-Ming Tsang ◽  
Cheng-Lung Hsu ◽  
...  
Keyword(s):  
Treatment Outcome ◽  
Nasopharyngeal Carcinoma ◽  
Tumor Progression

scholarly journals Protein N-arginine methyltransferase 5 promotes the tumor progression and radioresistance of nasopharyngeal carcinoma

2015 ◽  
Vol 35 (3) ◽  
pp. 1703-1710 ◽  
Author(s):  
DAOKE YANG ◽  
TIANSONG LIANG ◽  
YUE GU ◽  
YULIN ZHAO ◽  
YONGGANG SHI ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Progression ◽  
Arginine Methyltransferase

CD10 expression by fusiform stromal cells in nasopharyngeal carcinoma correlates with tumor progression

2006 ◽  
Vol 449 (2) ◽  
pp. 220-224 ◽  
Author(s):  
Hend Braham ◽  
Mounir Trimeche ◽  
Sonia Ziadi ◽  
Sarra Mestiri ◽  
Moncef Mokni ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Progression ◽  
Stromal Cells ◽  
Cd10 Expression

Recurrent chemical reactivations of EBV promotes genome instability and enhances tumor progression of nasopharyngeal carcinoma cells

2009 ◽  
Vol 124 (9) ◽  
pp. 2016-2025 ◽  
Author(s):  
Chih-Yeu Fang ◽  
Chia-Huei Lee ◽  
Chung-Chun Wu ◽  
Yu-Ting Chang ◽  
Shu-Ling Yu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Progression ◽  
Genome Instability ◽  
Carcinoma Cells

scholarly journals Dual PI3K/mTOR Inhibitors, GSK2126458 and PKI-587, Suppress Tumor Progression and Increase Radiosensitivity in Nasopharyngeal Carcinoma

2014 ◽  
Vol 14 (2) ◽  
pp. 429-439 ◽  
Author(s):  
Tongxin Liu ◽  
Quanquan Sun ◽  
Qi Li ◽  
Hua Yang ◽  
Yuqin Zhang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Progression ◽  
Mtor Inhibitors

scholarly journals Exosomes overexpressing miR-34c inhibit malignant behavior and reverse the radioresistance of nasopharyngeal carcinoma

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Fang-Zhu Wan ◽  
Kai-Hua Chen ◽  
Yong-Chu Sun ◽  
Xi-Chan Chen ◽  
Ren-Ba Liang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Suppressor ◽  
Tumor Progression ◽  
Epithelial Mesenchymal Transition ◽  
Luciferase Reporter ◽  
Serum Samples ◽  
Mesenchymal Transition ◽  
Malignant Behavior

Abstract Background Malignant behavior and radioresistance, which severely limits the efficacy of radiation therapy (RT) in nasopharyngeal carcinoma (NPC), are associated with tumor progression and poor prognosis. Mesenchymal stem cells (MSCs) are used as a therapeutic tool in a variety of tumors. The aim of this study was to reveal the effect of tumor suppressor microRNA-34c-5p (miR-34c) on NPC development and radioresistance, as well as to confirm that exosomes derived from MSCs overexpressing miR-34c restore the sensitivity to radiotherapy in NPCs. Methods Potentially active microRNAs were screened by cell sequencing, Gene Expression Omnibus (GEO) database analysis, and analysis of clinical serum samples from 70 patients. The expression of genes and proteins was detected by Western blotting, quantitative reverse transcription PCR (qRT-PCR), and immunohistochemistry (IHC). Proliferation, apoptosis, invasion, migration and radioresistance of NPC were detected. Luciferase reporter assays were used to verify the interactions of microRNAs with their downstream targets. MSCs exosomes were isolated by ultrafiltration and verified by electron microscopy and nanoparticle tracking technology. Results The expression of miR-34c was associated with the occurrence and radiation resistance of NPC. In vitro and in vivo experiments indicated that overexpression of miR-34c inhibit malignant behavior such as invasion, migration, proliferation and epithelial-mesenchymal transition (EMT) in NPCs by targeting β-Catenin. In addition, we found alleviated radioresistance upon miR-34c overexpression or β-catenin knockdown in NPCs. Exosomes derived from miR-34c-transfected MSCs attenuated NPC invasion, migration, proliferation and EMT. Moreover, miR-34c-overexpressing exosomes drastically increased radiation-induced apoptosis in NPC cells. Conclusion miR-34c is a tumor suppressor miR in NPC, which inhibits malignant behavior as well as radioresistance of tumor. Therefore, exogenous delivery of miR-34c to NPCs via MSC exosomes inhibits tumor progression and increases the efficiency of RT. Combination IR with miR-34c-overexpressing exosomes may be effective treatment for radioresistant NPCs.

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