IGFL2-AS1 facilitates tongue squamous cell carcinoma progression via Wnt/β-catenin signaling pathway

被引:18
|
作者
Zhao, Ruimin [1 ]
Wang, Shiyang [1 ]
Tan, Lu [2 ]
Li, Huajing [1 ]
Liu, Junsong [1 ]
Zhang, Shaoqiang [1 ]
机构
[1] Xi An Jiao Tong Univ, Dept Otorhinolaryngol Head & Neck Surg, Affiliated Hosp 1, 277 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Dept Pediat, Affiliated Hosp 1, Xian, Peoples R China
关键词
IGFL2-AS1; SATB1; tongue squamous cell carcinoma; Wnt/beta-catenin; PROLIFERATION; INVASION; SUPPRESSES; EXPRESSION; MIGRATION; PROGNOSIS; SATB1; RNAS;
D O I
10.1111/odi.13935
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Objectives: Tongue squamous cell carcinoma (TSCC) is the most common malignancy in oral cancer. Long noncoding RNAs (lncRNAs) are important regulators in cancer biology. In our present study, we investigated a novel lncRNA IGF-like family member 2 antisense RNA 1 (IGFL2-AS1) in TSCC. Methods: RT-qPCR analyzed IGFL2-AS1 expression in TSCC cells. Functional assays assessed the impact of IGFL2-AS1 on TSCC cell proliferation, migration, and invasion. Western blot analyzed the protein levels of EMT-related markers. Mechanism assays analyzed the regulatory mechanism of IGFL2-AS1 in TSCC cells. In-vivo experiments were conducted to prove the role of IGFL2-AS1 in TSCC progression. Results: IGFL2-AS1 was significantly up-regulated in TSCC cells and tissues, and IGFL2-AS1 knockdown inhibited cell proliferation, migration, invasion and EMT in TSCC. Moreover, IGFL2-AS1 functioned as a competing endogenous RNA (ceRNA) to sponge miR-1224-5p and thereby modulated SATB homeobox 1 (SATB1) expression. Additionally, SATB1 activated the Wnt/beta-catenin signaling pathway in TSCC cells and IGFL2-AS1 regulated the Wnt/beta-catenin signaling pathway and TSCC progression via elevating SATB1 expression. Conclusions: The data revealed that IGFL2-AS1 played a cancer promoting role in TSCC and may aid in exploring a brand new biomarker that might contribute to TSCC treatment.
引用
收藏
页码:469 / 482
页数:14
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