Modified Panax ginseng extract regulates autophagy by AMPK signaling in A549 human lung cancer cells
| Autor: | Hwa-Seung Yoo, Jung Min Kim, Pei Ying Yang, Min Goo Lee, Seung Yeul Lee, Ik Soon Jang, Chong-Kwan Cho, Hwan Su Kang, Eunbi Jo |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Cancer Research Lung Neoplasms ATG5 Panax Cell Cycle Proteins Biology AMP-Activated Protein Kinases 03 medical and health sciences chemistry.chemical_compound Ginseng 0302 clinical medicine Autophagy Humans PI3K/AKT/mTOR pathway Adaptor Proteins Signal Transducing Protopanaxatriol A549 cell Oncogene Plant Extracts TOR Serine-Threonine Kinases AMPK General Medicine Saponins Phosphoproteins Cell biology Gene Expression Regulation Neoplastic 030104 developmental biology Oncology chemistry A549 Cells 030220 oncology & carcinogenesis Cancer research Beclin-1 Microtubule-Associated Proteins Signal Transduction |
| Zdroj: | Oncology reports. 37(6) |
| ISSN: | 1791-2431 |
| Popis: | Panax ginseng has been used worldwide as a traditional medicine for the treatment of cancer and other diseases. The antiproliferative activity of ginseng has been increased after enzymatic processing of ginseng saponin, which may result in the accumulation of minor saponins, such as Rh2, Rg3, compound K and protopanaxatriol type (PPT) in modified regular ginseng extract (MRGX). In the present study, the anticancer activity and the associated mechanisms of MRGX were investigated using A549 human lung cancer cells. To elucidate the mechanisms underlying the effects of MRGX, we performed a microarray analysis of gene expression in the A549 cells. Molecular mechanisms that were associated with the anticancer activity of MRGX were studied, with a special focus on the autophagy-related multiple signaling pathways in lung cancer cells. Microarray analyses elucidated autophagy-related genes affected by MRGX. Administration of MRGX at 100 µg/ml induced punctate cytoplasmic expression of LC3, Beclin-1 and ATG5 and increased expression of endogenous LC3-II whereas 50 µg/ml did not inhibit the proliferation of A549 cells. Compared to the control cells, in cells treated with MRGX at 100 µg/ml, the level of p-Akt was increased, while that of mTOR-4EBP1 was decreased. Downregulation of mTOR and 4EBP1 in the MRGX-treated cells was found not to be a p-Ulk (S757)-dependent pathway, but a p-Ulk (S317)-dependent autophagic pathway, using AMPK. These data suggest that MRGX regulates AMPK and induces autophagy in lung cancer cells. |
| Databáze: | OpenAIRE |
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