scholarly journals Role of polymorphic Fc gamma receptor IIIa and EGFR expression level in cetuximab mediated, NK cell dependent in vitro cytotoxicity of head and neck squamous cell carcinoma cells

2009 ◽  
Vol 58 (11) ◽  
pp. 1863-1864 ◽  
Author(s):  
Andrés López-Albaitero ◽  
Steve C. Lee ◽  
Sarah Morgan ◽  
Jennifer R. Grandis ◽  
William E. Gooding ◽  
...  
2009 ◽  
Vol 58 (11) ◽  
pp. 1853-1862 ◽  
Author(s):  
Andrés López-Albaitero ◽  
Steve C. Lee ◽  
Sarah Morgan ◽  
Jennifer R. Grandis ◽  
William E. Gooding ◽  
...  

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xiaofeng Qi ◽  
Wengguang Xu ◽  
Junqi Xie ◽  
Yufeng Wang ◽  
Shengwei Han ◽  
...  

Abstract Resistance towards chemotherapy is a common complication in treatment of oral cancers, which leads to treatment failure and poor outcome. In recent years, a growing body of evidence has shown that tumour hypoxia significantly contributes to chemoresistance. Metformin, a widely used oral hypoglycaemic drug, can reportedly potentiate the efficacy of chemotherapeutic drugs in various cancers; however, the underlying mechanisms are intricate and have not been fully understood. In this study, we explored the role of metformin in chemosensitivity of oral squamous cell carcinoma cells (OSCC) to cisplatin both in vitro and in vivo, and attempted to elucidate its possible underlying mechanisms. Encouragingly, we found that metformin synergistically enhanced cisplatin cytotoxicity and reversed the chemoresistance to certain extent. This mechanism could likely be related with inhibition of the NF-κB/HIF-1α signal axis and lead to the downregulation of hypoxia-regulated genes products. Therefore, metformin could serve as a chemosensitiser for cisplatin-based regimens for OSCC, thereby providing a theoretical basis for future use in the treatment of oral cancers.


Toxins ◽  
2015 ◽  
Vol 8 (1) ◽  
pp. 7 ◽  
Author(s):  
Thao Nguyen ◽  
Marie-Odile Parat ◽  
Mark Hodson ◽  
Jenny Pan ◽  
Paul Shaw ◽  
...  

2005 ◽  
Vol 17 (2) ◽  
pp. 105-113 ◽  
Author(s):  
Takashi Hase ◽  
Shuichi Kawashiri ◽  
Akira Tanaka ◽  
Shinichi Nozaki ◽  
Natsuyo Noguchi ◽  
...  

2003 ◽  
Vol 52 (2) ◽  
pp. 107-115 ◽  
Author(s):  
Mikel B. Moore ◽  
Zoya B. Kurago ◽  
Colleen A. Fullenkamp ◽  
Charles T. Lutz

2021 ◽  
Author(s):  
Jiao Jiao Hu ◽  
Yu Ji ◽  
Ting Ting Miao ◽  
Shi Yao Zheng ◽  
Xiao Bin Cui ◽  
...  

Abstract BackgroundEsophageal squamous cell carcinoma (ESCC) is one of the most lethal malignancies. Increasing evidence has revealed that Human Papillomavirus (HPV) infection may be associated with the possible etiology of ESCC. Nevertheless, the precise role of HPV in ESCC remains unclear.MethodsProliferation and apoptosis capability of ESCC cells upon infection of HPV16 E6 were detected by CCK-8 assay and Western blotting analysis. Wound healing assay and Transwell experiment were conducted to determine the ability of migration and invasion, and the mRNA expression of E6AP, p53, miR-34a was determined by real-time PCR after transfected with HPV16 E6 plasmid. ResultsIn ESCC cells, the ability of proliferation, migration and invasion were increased, and the ability of apoptosis was decreased after transfected with HPV16 E6 plasmid. Furthermore, the mRNA level of E6AP, P53 and miR-34a were decreased in HPV16 E6-transfected cell lines.ConclusionsOur results not only provide evidence that in ESCC, HPV16 E6 promotes cell proliferation, migration and invasion, inhibits cell apoptosis, but also suggest that there may be a correlation between E6AP, P53 and miR-34a in HPV-transfected cell lines. These findings indicated that HPV16 E6 may play an important role in the development of ESCC.


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