{"title":"转录因子TP63通过上调KRT17表达,诱导上皮-间质转化,促进甲状腺癌的恶性进展。","authors":"Fanbo Meng, Liting Dai","doi":"10.1080/08977194.2023.2184656","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8000,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Transcription factors TP63 facilitates malignant progression of thyroid cancer by upregulating KRT17 expression and inducing epithelial-mesenchymal transition.\",\"authors\":\"Fanbo Meng, Liting Dai\",\"doi\":\"10.1080/08977194.2023.2184656\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":12782,\"journal\":{\"name\":\"Growth factors\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2023-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Growth factors\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1080/08977194.2023.2184656\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/3/15 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Growth factors","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/08977194.2023.2184656","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/3/15 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
Transcription factors TP63 facilitates malignant progression of thyroid cancer by upregulating KRT17 expression and inducing epithelial-mesenchymal transition.
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.
期刊介绍:
Growth Factors is an international and interdisciplinary vehicle publishing new knowledge and findings on the regulators of cell proliferation, differentiation and survival. The Journal will publish research papers, short communications and reviews on current developments in cell biology, biochemistry, physiology or pharmacology of growth factors, cytokines or hormones which improve our understanding of biology or medicine. Among the various fields of study topics of particular interest include: •Stem cell biology •Growth factor physiology •Structure-activity relationships •Drug development studies •Clinical applications