COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1

被引:7
|
作者
Tian, Xiaobei [1 ,2 ]
Sun, Jian [1 ,2 ]
Li, Changshun [1 ,2 ]
Zhang, Kun [1 ,2 ]
机构
[1] Xuzhou Med Univ, Affiliated Stomatol Hosp, 130 Huaihai West Rd, Xuzhou 221004, Jiangsu, Peoples R China
[2] Xuzhou Med Univ, Sch Stomatol, Xuzhou 221004, Jiangsu, Peoples R China
关键词
collagen type IV alpha 1 chain; nidogen-1; oral squamous cell carcinoma; epithelial-mesenchymal transition; metastasis; CANCER; METASTASIS;
D O I
10.3892/etm.2023.11875
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Collagen type IV a1 chain (COL4A1) is a collagen protein that acts as a tumor-promoting factor in several types of cancer. However, the role and the potential mechanisms involving COL4A1 in oral squamous cell carcinoma (OSCC) remain unclear. Using reverse transcription-quantitative PCR and western blotting, the expression levels of COL4A1 and (nidogen-1) NID1 in OSCC cells were assessed. Cell Counting Kit-8, EdU staining and colony formation assays were used to evaluate cell proliferation. Cell migration and invasion were assessed using wound healing and Transwell invasion assays, respectively. The expression levels of proteins involved in epithelial-mesenchymal transition (EMT) were assessed using western blotting. In addition, the association between COL4A1 and NID1 was analyzed using TNMplot and the STRING database and verified by co-immunoprecipitation analysis. COL4A1 expression was found to be significantly increased in OSCC cells. Knockdown of COL4A1 expression decreased SCC-4 cell proliferation, migration and invasion, as well as the progression of EMT. In addition, COL4A1 was shown to be significantly positively associated with NID1 in OSCC and to bind to NID1. NID1 overexpression reversed the inhibitory effects of COL4A1 knockdown on cell proliferation, migration and invasion as well as on the progression of EMT in OSCC cells. In summary, the present findings demonstrated that COL4A1 promoted cell proliferation and migration as well as the progression of EMT in OSCC cells by binding to NID1, highlighting a potential avenue for therapeutic management of OSCC.
引用
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页数:9
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