The effect of TLR4/MyD88/NF-κB signaling pathway on proliferation and apoptosis in human nasopharyngeal carcinoma 5-8F cells induced by LPS.
- Author:
Yanwei LI
;
Guangru XIE
;
Ling LI
;
Zhangshen JIANG
;
Zhensong YUE
;
Zhanyu PAN
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Carcinoma;
Cell Cycle;
Cell Line, Tumor;
Cell Proliferation;
Gene Expression Regulation, Neoplastic;
Humans;
Myeloid Differentiation Factor 88;
metabolism;
NF-kappa B p50 Subunit;
metabolism;
Nasopharyngeal Carcinoma;
Nasopharyngeal Neoplasms;
pathology;
Signal Transduction;
Toll-Like Receptor 4;
metabolism
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2015;29(11):1012-1015
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To evaluate the effects of NF-κB activation on the proliferation and apoptosis throughTLR4/MyD88 signaling pathway in human nasopharyngeal carcinoma (NPC) 5-8F cell lines.
METHOD:TLR4 induced by LPS is inhibited by PE anti-human. Real-Time Quantitative PCR and Western blot were employed to evaluate the efficacy of mRNA level and protein expression. The growth inhibition rate of 5-8F by Celecoxib was evaluated with MTT method. The cell cycle and apoptosis were measured with flow cytometric method (FCM).
RESULT:By using the specific inhibitor, the protein and gene expression of NF-κB and MyD88 were both significantly lower than the control group (P<. 05). Meanwhile, the down-rugulation of NF-κB could inhibit proliferation of NPC 5-8F cells and promote their apoptosis (P<0. 05).
CONCLUSION:By inhibiting TLR4 / MyD88 signaling pathway, the expression of NF-κB in NPC 5-8F cells could decrease, then the cell proliferation was inhibited and cell apoptosis was induced. The results showed that TLR4 / MyD88 / NF-κB induced by LPS is an important pathway in the genesis and development of NPC. This study provides evidence for targeting research of NPC.
