1. Academic Validation
  2. Aquaporin 3 maintains the stemness of CD133+ hepatocellular carcinoma cells by activating STAT3

Aquaporin 3 maintains the stemness of CD133+ hepatocellular carcinoma cells by activating STAT3

  • Cell Death Dis. 2019 Jun 13;10(6):465. doi: 10.1038/s41419-019-1712-0.
Yawei Wang 1 Gang Wu 2 Xueyan Fu 3 Shaolin Xu 3 Tianlong Wang 1 Qi Zhang 1 Ye Yang 1
Affiliations

Affiliations

  • 1 Department of Geriatric Surgery, The First Affiliated Hospital of China Medical University, Shenyang, PR China.
  • 2 Department of Hepatobiliary Surgery, The First Affiliated Hospital of China Medical University, Shenyang, PR China. [email protected].
  • 3 Department of Hepatobiliary Surgery, The First Affiliated Hospital of China Medical University, Shenyang, PR China.
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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