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.
emerging evidence suggests that long noncoding rnas (lncrnas) serve a key role in malignant transformation, tumor progression and metastasis. increased expression of lncrna p53 upregulated regulator of P53 levels (PurPl) has been reported to promote tumorigenicity in colorectal cancer; however, the role and potential mechanisms of PurPl in the development of liver cancer remain unclear. We employed reverse transcription-quantitative polymerase chain reaction to detect PurPl and p53 mrna expression in liver cancer tissues and cell lines. cell counting Kit-8 and colony-forming assays were used to examine the cell proliferation; whereas, flow cytometry was applied to detect apoptosis and cell cycle progression. p53 expression was detected by western blotting. The results revealed that PURPL was significantly upregulated in liver cancer tissues compared with in paracancerous tissues, and was associated with tumor differentiation stage and tumor size. PurPl was also upregulated in various liver cancer cell lines. Silencing of PurPl inhibited liver cancer cells proliferation, blocked cell cycle progression, and promoted apoptosis. Most importantly, PurPl expression was negatively correlated with p53 mrna expression. in summary, lncrna-PurPl was proposed to promote cell proliferation in liver cancer by regulating the p53 gene. as such, it could serve as a potential therapeutic target for the diagnosis and treatment of liver cancer.
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