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Lutein Inhibits Cell Growth and Activates Apoptosis via the PI3K/AKT/mTOR Signaling Pathway in A549 Human Non-Small-Cell Lung Cancer Cells.
Journal of Environmental Pathology, Toxicology and Oncology ( IF 2.1 ) Pub Date : 2019-02-27 , DOI: 10.1615/jenvironpatholtoxicoloncol.2018027418
Wen-Long Zhang 1 , Ya-Nan Zhao 1 , Zhang-Zhen Shi 1 , Dan Cong 1 , Yuan-Song Bai 1
Affiliation  

Cancer, the uncontrolled growth of cells, is a major disease that threatens the worldwide population. Among all cancer types, lung cancer has the highest morbidity rate, with a survival rate of less than 5%. Various studies have focused on discovering a potent anticancer drug that will increase the survival rate of lung cancer patients. Lutein (3,3'-dihydroxy-β, ε-carotene), a carotenoid present in fruits and vegetables, is one such compound that possesses excellent antioxidant properties. The present study was designed to determine the anticancer effect of lutein against A549, a non-small-cell lung cancer cell line. The cytotoxic effect of lutein against lung cancer cells (A549 and HCC827) and normal cells (BEAS-2B) was detected by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. The Transwell assay was performed to detect the inhibitory potential of lutein against cell invasion and migration of A549 cells. The induction of apoptosis by lutein in A549 was analyzed by a double-staining technique using TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling) and DAPI (4',6-diamidino-2-phenylindole) staining assays to confirm the molecular mechanism exhibited by lutein to induce apoptosis through regulating the phosphoinositide 3-kinase (PI3K)/AKT signaling molecules that are often deregulated in cancerous condition. The results show that lutein inhibits the PI3K/AKT signaling pathway and induces apoptosis in A549, which may therefore be used as a potent natural anticancer drug with no side effects to treat lung cancer.

中文翻译:

叶黄素通过A549人非小细胞肺癌细胞中的PI3K / AKT / mTOR信号通路抑制细胞生长并激活细胞凋亡。

癌症是细胞不受控制的生长,是威胁全球人口的主要疾病。在所有癌症类型中,肺癌的发病率最高,存活率低于5%。各种研究都集中在发现有效的抗癌药物上,该药物将增加肺癌患者的生存率。叶黄素(3,3'-二羟基-β,ε-胡萝卜素)是一种存在于水果和蔬菜中的类胡萝卜素,是一种此类化合物,具有出色的抗氧化性能。本研究旨在确定叶黄素对非小细胞肺癌A549细胞的抗癌作用。叶黄素对肺癌细胞(A549和HCC827)和正常细胞(BEAS-2B)的细胞毒性作用通过MTT(3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物)测定法检测。进行Transwell分析以检测叶黄素对A549细胞侵袭和迁移的抑制潜力。通过双染色技术,使用TUNEL(末端脱氧核苷酸转移酶介导的dUTP缺口末端标记)和DAPI(4',6-diamidino-2-phenylindole)染色法分析叶黄素对A549细胞凋亡的诱导作用,以确认其分子机制叶黄素显示出通过调节磷酸肌醇3-激酶(PI3K)/ AKT信号分子诱导细胞凋亡的作用,而这种信号分子通常在癌性状态下会失活。结果表明,叶黄素抑制PI3K / AKT信号通路并诱导A549中的细胞凋亡,因此可以用作有效的天然抗癌药物,而没有副作用来治疗肺癌。
更新日期:2019-11-01
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