BOS-93, a novel bromophenol derivative, induces apoptosis and autophagy in human A549 lung cancer cells via PI3K/Akt/mTOR and MAPK signaling pathway
文献类型：期刊论文
| 作者 | Guo, Chuanlong1,2; Wang, Lijun1,2; Zhao, Yue1,2; Jiang, Bo1,2; Luo, Jiao1,2; Shi, Dayong1,2 |
| 刊名 | EXPERIMENTAL AND THERAPEUTIC MEDICINE
 |
| 出版日期 | 2019-05-01 |
| 卷号 | 17期号:5页码:3848-3858 |
| ISSN号 | 1792-0981 |
| 关键词 | bromophenol apoptosis autophagy phosphoinositide 3-kinase protein kinase B mechanistic target of rapamycin signaling reactive oxygen species |
| DOI | 10.3892/etm.2019.7402 |
| 通讯作者 | Shi, Dayong(shidayong@qdio.ac.cn) |
| 英文摘要 | The novel bromophenol derivative, 3-(3-bromo-5-methoxy-4-(3-(piperidin-1-yl)propoxy)benzylidene)-N-(4-bromophenyl)-2-oxoindoline-5-sulfonamide (BOS-93), was synthesized in the CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences (Qingdao, China). Experimental studies have demonstrated that it could induce apoptosis and autophagy in human A549 lung cancer cells, and it could also inhibit tumor growth in human A549 lung cancer xenograft models. In the present study, the molecular pathways underlying these effects were identified. The results demonstrated that BOS-93 could inhibit cell proliferation in A549 cells and block A549 cells at the G0/G1 phase. Furthermore, BOS-93 could induce apoptosis, activate caspase-3 and poly ADP ribose polymerase, and increase the B cell lymphoma (Bcl)-2 associated X protein/Bcl-2 ratio. Notably, BOS-93 could also induce autophagy in A549 cells. BOS-93-induced autophagy was confirmed by detecting light chain 3 (LC3)-I/LC3-II conversion and increasing expression of beclin1 and autophagy-related gene 14. Notably, BOS-93-induced autophagy could be inhibited by the autophagy inhibitor 3-MA. Flow cytometry, transmission electron microscopy (TEM) and western blot analysis indicated that BOS-93 induced apoptosis and autophagy activities by deactivating phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin and activating the mitogen-activated protein kinase signaling pathway. The present findings indicated that BOS-93 might be a novel anti-cancer agent for treatment of human lung cancer. |
| 资助项目 | National Natural Science Foundation of China[81773586] ; National Natural Science Foundation of China[81703354] ; Key Research Program of Frontier Sciences, CAS[QYZDB-SSW-DQC014] ; Project of Discovery, Evaluation and Transformation of Active Natural Compounds, Strategic Biological Resources Service Network Programme of Chinese Academy of Sciences[ZSTH-026] ; Shandong Provincial Natural Science Foundation for Distinguished Young Scholars[JQ201722] ; National Program for Support of Top-notch Young Professionals ; Taishan Scholar Youth Project of Shandong Province |
| WOS研究方向 | Research & Experimental Medicine |
| 语种 | 英语 |
| 出版者 | SPANDIDOS PUBL LTD |
| WOS记录号 | WOS:000466935600072 |
| 源URL | [http://ir.qdio.ac.cn/handle/337002/161258]  |
| 专题 | 海洋研究所_实验海洋生物学重点实验室 |
| 通讯作者 | Shi, Dayong |
| 作者单位 | 1.Chinese Acad Sci, Inst Oceanol, CAS Key Lab Expt Marine Biol, 7 Nanhai Rd, Qingdao 266071, Shandong, Peoples R China 2.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Drugs & Bioprod, Qingdao 266071, Shandong, Peoples R China |
| 推荐引用方式 GB/T 7714 | Guo, Chuanlong,Wang, Lijun,Zhao, Yue,et al. BOS-93, a novel bromophenol derivative, induces apoptosis and autophagy in human A549 lung cancer cells via PI3K/Akt/mTOR and MAPK signaling pathway[J]. EXPERIMENTAL AND THERAPEUTIC MEDICINE,2019,17(5):3848-3858. |
| APA | Guo, Chuanlong,Wang, Lijun,Zhao, Yue,Jiang, Bo,Luo, Jiao,&Shi, Dayong.(2019).BOS-93, a novel bromophenol derivative, induces apoptosis and autophagy in human A549 lung cancer cells via PI3K/Akt/mTOR and MAPK signaling pathway.EXPERIMENTAL AND THERAPEUTIC MEDICINE,17(5),3848-3858. |
| MLA | Guo, Chuanlong,et al."BOS-93, a novel bromophenol derivative, induces apoptosis and autophagy in human A549 lung cancer cells via PI3K/Akt/mTOR and MAPK signaling pathway".EXPERIMENTAL AND THERAPEUTIC MEDICINE 17.5(2019):3848-3858. |
入库方式： OAI收割
来源：海洋研究所
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