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Antiproliferative effect of the methanol extract from the roots of Petasites japonicus on Hep3B hepatocellular carcinoma cells in vitro and in vivo
Author(s) -
Hyun Jung Kim,
Song Yi Park,
Hye Min Lee,
Dong Ik Seo,
YoungMin Kim
Publication year - 2015
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2015.2296
Subject(s) - protein kinase b , viability assay , pi3k/akt/mtor pathway , wnt signaling pathway , mtt assay , in vivo , hepatocellular carcinoma , cell cycle , cell growth , traditional medicine , cell , western blot , biology , oncogene , chemistry , pharmacology , cancer research , apoptosis , signal transduction , biochemistry , medicine , microbiology and biotechnology , gene
Traditional medicinal plants have been used in the treatment of various diseases for centuries. A number of plant-derived compounds have been proposed as anticancer agents and are currently undergoing medical development. Petasites japonicus (PJ), also known as Butterbur, is a herb cultivated in East Asia that is used as a traditional herbal medicine. The aim of the present study was to investigate whether a methanol extract of PJ demonstrated anticancer activity against Hep3B hepatocellular carcinoma (HCC) cells. The anticancer property and underlying mechanism of the extract were evaluated by assessing the effect on cell viability, nuclear morphology and the expression of phosphorylated (p)-mTOR, p-Akt, β-catenin and p-glycogen synthase kinase-3β, which are markers for cancer cell proliferation and metastasis. These results were obtained by the MTT assay, fluorescence microscopy and Western blot analysis. The methanol extract of PJ was shown to decrease the cell viability in a concentration-dependent manner. In addition, the methanol extract of PJ was found to inhibit the growth of Hep3B HCC cells through inhibiting the Akt/mTOR and Wnt signaling pathways. These results suggest that the methanol extract of PJ exerts an anticancer effect on Hep3B HCC cells.

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