HOXC10 promotes nasopharyngeal carcinoma cell proliferation and migration by regulating PI3K/AKT pathway

被引:1
|
作者
Wu, Liping [1 ]
Qian, Guohong [2 ]
Zheng, Yuqing [3 ]
Zheng, Huizhen [4 ]
机构
[1] Huzhou Univ, Huzhou Cent Hosp, Dept Otolaryngol, Huzhou 313000, Zhejiang, Peoples R China
[2] Huzhou Univ, Huzhou Cent Hosp, Dept Otolaryngol, Huzhou 313000, Zhejiang, Peoples R China
[3] Huzhou Univ, Sch Engn, Huzhou 313000, Zhejiang, Peoples R China
[4] Shanghai Univ, Wenzhou Peoples Hosp, Affiliated Hosp 3, Dept Otolaryngol, Wenzhou 325000, Zhejiang, Peoples R China
关键词
HOXC10; Nasopharyngeal carcinoma; Cell proliferation; Cell migration; Invasion; PI3K; AKT; BREAST-CANCER; POOR SURVIVAL; METASTASIS; EXPRESSION; OVEREXPRESSION; ACTIVATION;
D O I
10.4314/tjpr.v21i8.3
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Purpose: To evaluate the role of homeobox C10 (HOXC10) in nasopharyngeal carcinoma (NPC).Methods: Cell Counting Kit-8 (CCK-8) and colony formation assays were conducted to determine NPC cell proliferation. Cell migration and invasion were assessed using a Transwell assay, while western blot was used to investigate the mechanism of action involved in HOXC10-mediated NPC.Results: HOXC10 levels were significantly elevated in NPC cells (p < 0.001). Over-expression of HOXC10 significantly increased NPC cell viability (p < 0.05) and proliferation. However, silencing HOXC10 reduced NPC cell proliferation. HOXC10 knockdown suppressed NPC cell migration and invasion. NPC expression of phosphorylated phosphoinositide-3-kinase (PI3K) and protein kinase B (AKT) proteins were up-regulated after HOXC10 over-expression but were down-regulated upon silencing HOXC10 (p < 0.05).Conclusion: HOXC10 knockdown reduces NPC cell proliferation and metastasis by inactivating PI3K/AKT pathway, and therefore, can potentially be developed for the treatment of nasopharyngeal carcinoma.
引用
收藏
页码:1595 / 1600
页数:6
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