TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling Pathway
TEEG (3β,16β,23-trihydroxy-13,28-epoxyurs-11-ene-3-O-β-D-glucopyranoside) is derived from the chloroform extract of the Chinese medicine formula Shenqi San (CE-SS). In the present study, we aimed to elucidate the anticancer effect and possible molecular mechanism underlying the action of TEEG agains...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2019-01-01
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| Series: | Analytical Cellular Pathology |
| Online Access: | http://dx.doi.org/10.1155/2019/7697610 |
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| _version_ | 1832567719422066688 |
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| author | Lu Shi Yijun Tu Yu Xia Siqi Ye Chaozhi Ma Yanwen Liu Pengtao You |
| author_facet | Lu Shi Yijun Tu Yu Xia Siqi Ye Chaozhi Ma Yanwen Liu Pengtao You |
| author_sort | Lu Shi |
| collection | DOAJ |
| description | TEEG (3β,16β,23-trihydroxy-13,28-epoxyurs-11-ene-3-O-β-D-glucopyranoside) is derived from the chloroform extract of the Chinese medicine formula Shenqi San (CE-SS). In the present study, we aimed to elucidate the anticancer effect and possible molecular mechanism underlying the action of TEEG against the human non-small cell lung cancer (NSCLC) cell line A549 in vitro. A549 cells were incubated with different concentrations of TEEG. Cell proliferation was assessed by MTT assay. Autophagy was evaluated by immunofluorescence staining. Autophagy-associated proteins were examined by Western blot analysis. TEEG markedly inhibited A549 cell proliferation in a concentration-dependent manner. Immunofluorescence staining showed that TEEG induced autophagy in A549 cells. The LC3-II : LC3-I conversion ratio and the expression of Beclin-1, Atg5, Atg7, and Atg12 increased with the concentration of TEEG. In addition, increased TEEG concentration enhanced the expression of Class III p-PI3K and reduced the expression of Class I p-PI3K, p-AKT, p-mTOR, and p-P70S6K. These results indicate that TEEG induces autophagy of A549 cells through regulation of the PI3K/AKT/mTOR signaling pathway. |
| format | Article |
| id | doaj-art-3d2946791b9c495284c86d07cfbe9327 |
| institution | Kabale University |
| issn | 2210-7177 2210-7185 |
| language | English |
| publishDate | 2019-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Analytical Cellular Pathology |
| spelling | doaj-art-3d2946791b9c495284c86d07cfbe93272025-02-03T01:00:40ZengWileyAnalytical Cellular Pathology2210-71772210-71852019-01-01201910.1155/2019/76976107697610TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling PathwayLu Shi0Yijun Tu1Yu Xia2Siqi Ye3Chaozhi Ma4Yanwen Liu5Pengtao You6Department of Pharmacy, Medical College, Jianghan University, Hubei, Wuhan 430056, ChinaHubei Key Laboratory of Resources and Chemistry of Chinese Medicine, Hubei University of Chinese Medicine, Hubei, Wuhan 430065, ChinaHubei Key Laboratory of Resources and Chemistry of Chinese Medicine, Hubei University of Chinese Medicine, Hubei, Wuhan 430065, ChinaDepartment of Dermatology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, ChinaHubei Key Laboratory of Resources and Chemistry of Chinese Medicine, Hubei University of Chinese Medicine, Hubei, Wuhan 430065, ChinaHubei Key Laboratory of Resources and Chemistry of Chinese Medicine, Hubei University of Chinese Medicine, Hubei, Wuhan 430065, ChinaHubei Key Laboratory of Resources and Chemistry of Chinese Medicine, Hubei University of Chinese Medicine, Hubei, Wuhan 430065, ChinaTEEG (3β,16β,23-trihydroxy-13,28-epoxyurs-11-ene-3-O-β-D-glucopyranoside) is derived from the chloroform extract of the Chinese medicine formula Shenqi San (CE-SS). In the present study, we aimed to elucidate the anticancer effect and possible molecular mechanism underlying the action of TEEG against the human non-small cell lung cancer (NSCLC) cell line A549 in vitro. A549 cells were incubated with different concentrations of TEEG. Cell proliferation was assessed by MTT assay. Autophagy was evaluated by immunofluorescence staining. Autophagy-associated proteins were examined by Western blot analysis. TEEG markedly inhibited A549 cell proliferation in a concentration-dependent manner. Immunofluorescence staining showed that TEEG induced autophagy in A549 cells. The LC3-II : LC3-I conversion ratio and the expression of Beclin-1, Atg5, Atg7, and Atg12 increased with the concentration of TEEG. In addition, increased TEEG concentration enhanced the expression of Class III p-PI3K and reduced the expression of Class I p-PI3K, p-AKT, p-mTOR, and p-P70S6K. These results indicate that TEEG induces autophagy of A549 cells through regulation of the PI3K/AKT/mTOR signaling pathway.http://dx.doi.org/10.1155/2019/7697610 |
| spellingShingle | Lu Shi Yijun Tu Yu Xia Siqi Ye Chaozhi Ma Yanwen Liu Pengtao You TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling Pathway Analytical Cellular Pathology |
| title | TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling Pathway |
| title_full | TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling Pathway |
| title_fullStr | TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling Pathway |
| title_full_unstemmed | TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling Pathway |
| title_short | TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling Pathway |
| title_sort | teeg induced a549 cell autophagy by regulating the pi3k akt mtor signaling pathway |
| url | http://dx.doi.org/10.1155/2019/7697610 |
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