Transcription factors TP63 facilitates malignant progression of thyroid cancer by upregulating KRT17 expression and inducing epithelial-mesenchymal transition

被引:3
作者
Meng, Fanbo [1 ]
Dai, Liting [2 ,3 ]
机构
[1] Shaoxing Univ, Dept Breast & Thyroid Surg, Affiliated Hosp, Shaoxing, Peoples R China
[2] Shaoxing Univ, Med Examinat Ctr, Affiliated Hosp, Shaoxing, Peoples R China
[3] Shaoxing Univ, Med Examinat Ctr, Affiliated Hosp, 999 Zhongxing South Rd, Shaoxing 312000, Peoples R China
关键词
Thyroid cancer; TP63; KRT17; epithelial-mesenchymal transition; progression; KERATIN; 17; CELL; PROLIFERATION; CARCINOMA; INVASION; P63; OVEREXPRESSION; METASTASIS; MIGRATION; PATHWAYS;
D O I
10.1080/08977194.2023.2184656
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Thyroid cancer (TC) is a relatively prevalent endocrine tumor among women, the incidence of which is rapidly rising. In this present study, we aimed to provide new therapeutic targets from the aspect of transcription factor-target gene interaction. TP63 and KRT17 were both highly expressed in TC tissues and cells. The results of ChIP and dual-luciferase assays confirmed TP63 to bind the KRT17 promoter. Cell function assays revealed that knockdown of TP63 could repress TC cell progression. Furthermore, the rescue assay verified that TP63 could facilitate KRT17 expression to activate the AKT signaling pathway, which in turn stimulated TC cell invasion and migration, and induced EMT. All these results verified that TP63 facilitates TC malignant progression by promoting KRT17 expression and inducing EMT.
引用
收藏
页码:71 / 81
页数:11
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