Relationship between the expression of TrkB and anoikis resistance in nasopharyngeal carcinoma line
10.3321/j.issn:1673-0860.2008.08.010
- VernacularTitle:鼻咽癌细胞株C666-1细胞中酪氨酸激酶受体B的表达与抗失巢凋亡的关系
- Author:
Wen-Sheng WEN
1
;
Zhe ZHANG
;
Ying XIE
;
Xiang YI
;
Wei-Min ZHAO
;
Zhi-Wen XU
;
An-Zhou TANG
;
Guang-Wu HUANG
Author Information
1. 广西医科大学附属第一医院
- Keywords:
Nasopharyngeal neoplasms;
Tumor cells,cultured;
Receptor,trkB;
Anoikis
- From:
Chinese Journal of Otorhinolaryngology Head and Neck Surgery
2008;43(8):606-611
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the regulation of anokis by tyrosine kinase receptor B(TrkB) in human nasopharyngeal carcinoma lines. Methods Expression levels of TrkB and brain-derived neurotrophic factor (BDNF) were evaluated by RT-PCR and Western blot. Colony formation ability of C666-1 was observed in soft agar. Proliferation rate and apoptosis, that change in cells by treating the TrkB inhibitor K252a and specificity ligand BDNF respectively under suspension culture, were measured by cell counting kit-8 (CCK-8) assay and the flow cytometry assay. The expression change of TrkB, BDNF and phosphorylation of serine threonine kinase (p-Akt) were investigated by Western blot analysis. Results TrkB and BDNF were identified in C666-1 cells. C666-1 cells could be decreased the proliferation of colony in soft agar by effect of K252a, but BDNF could make the colony prolific. K252a can inhibit the expression of TrkB in C666-1, and prevent p-Akt activation. And exogenous BDNF stimulated up-regulation TrkB and p-Akt, induced anokis resistance. Conclusion TrkB inhibits anoikis in nasopharyngeal carcinoma cells. Inhibiton of TrkB by K252a can induce anoikis, and may prove particularly effective in treatment of nasopharyngeal carcinoma.
