WDR5 promotes the tumorigenesis of oral squamous cell carcinoma via CARM1/β-catenin axis

被引:6
|
作者
Lyu, Xiao-Ying [1 ]
Shui, Yu-Sen [1 ]
Wang, Liang [1 ]
Jiang, Qing-Song [1 ]
Meng, Ling-Xi [1 ]
Zhan, Hao-Yuan [2 ]
Yang, Ran [1 ]
机构
[1] Sichuan Univ, West China Hosp Stomatol, Natl Clin Res Ctr Oral Dis, State Key Lab Oral Dis, 14 Renmin South Rd, Chengdu 610065, Sichuan, Peoples R China
[2] Sichuan Univ, Chengdu 610065, Sichuan, Peoples R China
基金
中国国家自然科学基金;
关键词
OSCC; WDR5; CARM1; beta-catenin; Oral cancer; BETA-CATENIN ACTIVITY; GROWTH; CARM1;
D O I
10.1007/s10266-021-00649-6
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Oral squamous cell carcinoma (OSCC) is a malignancy all over the world. WD repeat domain 5 (WDR5) is involved in cancer progression. In addition, it was reported that WDR5 is upregulated in head and neck cancer, while its role in OSCC is unknown. First, the expression of WDR5 in oral cancer tissues and cells was examined by qRT-PCR, IHF and western blot. CCK-8 assay was performed to test the cell viability. Cell migration was assessed by transwell assay. Knocking down WDR5 or CARM1 in oral cancer cells to detect its function on cancer growth, WDR5 and CARM1 were significantly upregulated in OSCC. Silencing WDR5 suppressed OSCC cell viability and migration. CARM1 level in OSCC cells was significantly inhibited by WDR5 downregulation, and CARM1 elevation could rescue the effect of WDR5 knockdown on tumorigenesis of OSCC. Moreover, silencing of WDR5 notably inactivated beta-catenin signaling pathway, while this phenomenon was restored by CARM1 overexpression. Silencing of WDR5 attenuated the tumorigenesis of OSCC via CARM1/beta-catenin axis. Thus, WDR5 might be a target for OSCC treatment.
引用
收藏
页码:138 / 147
页数:10
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