Extract of L. Inhibits the Progression of Hepatocellular Carcinoma by Regulating and Pathway.

Hepatocellular carcinoma (HCC) poses a growing threat to humans due to poor prognosis. Extract of L. (ESC) is reported to inhibit metastasis of HCC. However, the underlying mechanism of ESC in regulating the progression of HCC needs to be further investigated. 3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to measure cell proliferation. Flow cytometry was employed to check cell apoptosis. Transwell assay was conducted to assess the abilities of cell migration and invasion. The protein levels of proliferating cell nuclear antigen, cleaved caspase 3 (c-caspase 3), E-cadherin, janus kinase 1 (JAK1), signal transducer and activator of transcription 3 (STAT3), and phosphorylated STAT3 were detected by Western blot. The interaction between and JAK1 was predicted by starBase, which was verified by the dual-luciferase reporter assay and RNA pull-down assay. The messenger RNA levels of and JAK1 were determined by quantitative real-time polymerase chain reaction. The results showed that the higher concentration or the longer time treatment of ESC led to the lower survival rate of HCC cells. Besides, ESC induced apoptosis and impeded migration and invasion of HCC cells. Moreover, downregulation of inverted the effects of ESC-mediated repression on HCC progression. Further studies indicated that targeted the 3'-untranslated region (3'UTR) of JAK1 and reversed JAK1-mediated impacts on HCC progression. Simultaneously, ESC inactivated pathway by regulating the expression of . ESC suppressed HCC progression by upregulating the expression of and blocking pathway.