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癌症干细胞
癌症研究
STAT蛋白
癌变
生物
干细胞
肝癌
细胞生物学
肝细胞癌
转录因子
化学
癌症
信号转导
基因
遗传学
作者
Yawei Wang,Gang Wu,Xueyan Fu,Shaolin Xu,Tianlong Wang,Qi Zhang,Ye Yang
标识
DOI:10.1038/s41419-019-1712-0
摘要
Abstract An increasing interest in liver cancer stemness arises owing to its aggressive behavior and poor prognosis. CD133, a widely known liver cancer stem cell marker, plays critical roles in the maintenance of liver cancer stemness. Thus, exploring the regulatory mechanism of CD133 expression is significant. In the present study, we proved the carcinogenesis roles of aquaporin 3 (AQP3) in hepatocellular carcinoma (HCC) and demonstrated that AQP3 promotes the stem cell-like properties of hepatoma cells by regulating CD133 expression. In addition, AQP3 promoted the stimulation and nuclear translocation of signal transducer and activator of transcription 3 (STAT3) with a subsequent increase in the level of CD133 promoter-acetylated histone H3. This phenomenon accelerated CD133 transcription. Next, whether AQP3 acted as an oncogenic gene in HCC and maintained the stemness of CD133+ hepatoma cells were elucidated; also, a novel mechanism underlying the AQP3/STAT3/CD133 pathway in HCC was deduced.
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