期刊
CYTOKINE
卷 148, 期 -, 页码 -出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2021.155649
关键词
HCC; Propofol; miR-105; JAK2; STAT3 signaling
The study found that Propofol significantly inhibited the proliferation of HCC cells and induced apoptosis by regulating the miR-105/JAK2/STAT3 signaling pathway. Therefore, Propofol may serve as a new therapeutic agent for HCC.
Background: Hepatocellular carcinoma (HCC) is a type of malignancy with high mortality. It has been reported Propofol could modulate the tumorigenesis of liver cancer; however, the mechanism by which Propofol regulates the development of HCC is still not clear. Methods: CCK8 assay was applied to test the cell viability. Flow cytometry and TUNEL staining were applied to detect the cell apoptosis. Meanwhile, dual luciferase reporter assay was performed to investigate the association between miR-105 and JAK2. In addition, RNA and protein levels were investigated by qRT-PCR and western blot, respectively. Results: Propofol significantly suppressed the proliferation of HCC cells via inducing the apoptosis. Consistently, miR-105 upregulation inhibited the proliferation of HCC cells, while downregulation of miR-105 reversed Propofol-induced HCC cell apoptosis. Meanwhile, JAK2 was found to be the direct target of miR-105. Furthermore, Propofol could inactivate JAK2/STAT3 signaling via upregulation of miR-105. Conclusion: Propofol significantly attenuated HCC tumorigenesis via mediation of miR-105/JAK2/STAT3 axis. Thereby, Propofol might act as a new agent for the treatment of HCC.
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