Background:Sanguisorba Officinalis L. (SO) is a well-known traditional Chinese medicine (TCM), commonly applied to treat complex diseases, such as anticancer, antibacterial, antiviral, anti-inflammatory, anti-oxidant and hemostatic effects. Especially, it has been reported to exert anti-tumor effect in various human cancers. However, its effect and pharmacological mechanism on hepatocellular carcinoma (HCC) remains unclear.Methods: In this study, network pharmacology approach was applied to characterize the underlying mechanism of SO on HCC. Active compounds and potential targets of SO, as well as related genes of HCC were obtained from the public databases, the potential targets and signaling pathways were determined by protein-protein interaction (PPI), gene ontology (GO) and pathway enrichment analyses. And the compound-target and target-pathway networks were constructed. Subsequently, in vitro experiments were also performed to further verify the anticancer effects of SO on HCC.Results: By using the comprehensive network pharmacology analysis, 41 ingredients in SO were collected from the corresponding databases, 12 active ingredients screened according to their oral bioavailability and drug-likeness index, and 258 potential targets related to HCC were predicted. Through enrichment analysis, SO was found to show its excellent therapeutic effects on HCC through several pathways, mainly related to proliferation and survival via the EGFR, PI3K/AKT, NFκB and MAPK signaling pathways. Additionally, in vitro, SO was found to inhibit cell proliferation, induce apoptosis and down-regulate cell migration and invasion in various HCC cells. Moreover, western blot analysis showed that SO treatment down-regulated the expression of p-EGFR, p-PI3K, p-AKT, p-NFκB and p-MAPK proteins in HepG2 cells. These results validated that SO exerted its therapeutic effects on HCC mainly by the regulation of cell proliferation and survival via the EGFR/MAPK and EGFR/PI3K/AKT/NFκB signaling pathways.Conclusion: Taken together, this study, revealed the anti-HCC effects of SO and its potential underlying therapeutic mechanisms in a multi-target and multi-pathway manner.

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Acute Myeloid Leukemia (AML) is a hematopoietic progenitor/stem cell disorder in which neoplastic myeloblasts are stopped at an immature stage of differentiation and lost the normal ability of proliferation and apoptosis. MicroRNAs (miRNAs) are small noncoding, single-stranded RNA molecules that can mediate the expression of target genes. While miRNAs mean to contribute the developments of normal functions, abnormal expression of miRNAs and regulations on their corresponding targets have often been found in the developments of AML and described in recent years. In leukemia, miRNAs may function as regulatory molecules, acting as oncogenes or tumor suppressors. Overexpression of miRNAs can down-regulate tumor suppressors or other genes involved in cell differentiation, thereby contributing to AML formation. Similarly, miRNAs can down-regulate different proteins with oncogenic activity as tumor suppressors. We herein review the current data on miRNAs, specifically their targets and their biological function based on apoptosis in the development of AML.