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Cancer: Nasopharyngeal Cancer
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Total 152 results found since Jan 2013.
Role of MIF/CXCL8/CXCR2 signaling in the growth of nasopharyngeal carcinoma tumor spheres
This study aims to evaluate the functions of MIF and CXCL8 on the growth of NPC tumor spheres. The elevated expression of CXCL8 in tumor over normal tissues was confirmed in 37 pairs of biopsies from NPC patients. In the in vitro study, all the poorly differentiated NPC cell lines, including the EBV-positive C666-1, and the EBV-negative CNE-1, CNE-2, SUNE-1, HNE-1 and HONE-1 cells, were found to express CXCL8 and MIF. Therefore, the EBV-positive C666-1 cell was selected to examine for the role of MIF and CXCL8 in the growth of the NPC tumor spheres. Functional study showed that the growth of C666-1 tumor spheres, under the...
Source: Cancer Letters - March 18, 2013 Category: Cancer & Oncology Authors: Ming-Chu Lo, Tak-Chun Yip, Kai-Cheong Ngan, Wai-Wai Cheng, Chun-Key Law, Pui-Shan Chan, King-Chi Chan, Chris Kong-Chu Wong, Ricky Ngok-Shun Wong, Kwok-Wai Lo, Wai-Tong Ng, Wing-Mui Lee, Sai-Wah Tsao, Lai-Wan Kwong, Maria Li Lung, Nai-Ki Mak Tags: Research Articles Source Type: research
Effects of Sam68 gene silencing on proliferation of nasopharyngeal carcinoma cell line 5-8F and its possible molecular mechanism.
Abstract
OBJECTIVE: To observe the effect of Sam68 gene silencing on proliferation of nasopharyngeal carcinoma (NPC) cell line 5-8F and explore its possible molecular mechanism.
METHODS: The NPC cell line 5-8F was transfected with a small interfering RNA (siRNA) targeting Sam68 and the cell proliferation changes were observed. Quantitative RT-PCR and Western blotting were used to examine the changes in the expressions of Sam68, cell cycle-related proteins, and some up-stream proteins in the transfected cells.
RESULTS: Transfection of 5-8F cells with Sam68-specific siRNA significantly lowered the mRNA and...
Source: Journal of Southern Medical University - February 1, 2013 Category: Universities & Medical Training Authors: Yang B, Feng DH Tags: Nan Fang Yi Ke Da Xue Xue Bao Source Type: research
