基因沉默
同源盒蛋白纳米
三阴性乳腺癌
癌症研究
癌变
Notch信号通路
生物
CDC42型
转移
纳米同源盒蛋白
癌症干细胞
波形蛋白
癌症
乳腺癌
细胞生物学
胚胎干细胞
干细胞
SOX2
信号转导
免疫学
诱导多能干细胞
遗传学
免疫组织化学
基因
作者
Yuan Tian,Peipei Zhang,Yajun Mou,Wenxiu Yang,Mengjie Zhang,Qing Li,Xiaowei Dou
标识
DOI:10.1038/s41420-023-01450-w
摘要
Abstract Elucidation of individual Notch protein biology in specific cancer is crucial to develop safe, effective, and tumor-selective Notch-targeting therapeutic reagents for clinical use [1]. Here, we explored the Notch4 function in triple-negative breast cancer (TNBC). We found that silencing Notch4 enhanced tumorigenic ability in TNBC cells via upregulating Nanog expression, a pluripotency factor of embryonic stem cells. Intriguingly, silencing Notch4 in TNBC cells suppressed metastasis via downregulating Cdc42 expression, a key molecular for cell polarity formation. Notably, downregulation of Cdc42 expression affected Vimentin distribution, but not Vimentin expression to inhibit EMT shift. Collectively, our results show that silencing Notch4 enhances tumorigenesis and inhibits metastasis in TNBC, indicating that targeting Notch4 may not be a potential strategy for drug discovery in TNBC.
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