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Journal of Environmental Pathology, Toxicology and Oncology
Импакт фактор: 1.241 5-летний Импакт фактор: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN Печать: 0731-8898
ISSN Онлайн: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2018027418
pages 341-350

Lutein Inhibits Cell Growth and Activates Apoptosis via the PI3K/AKT/mTOR Signaling Pathway in A549 Human Non-Small-Cell Lung Cancer Cells

Wen-long Zhang
Department of Hematology and Oncology, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, China, 130033
Ya-nan Zhao
Department of Hematology and Oncology, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, China, 130033
Zhang-zhen Shi
Department of Hematology and Oncology, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, China, 130033
Dan Cong
Department of Hematology and Oncology, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, China, 130033
Yuan-Song Bai
Department of Hematology and Oncology, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, China, 130033

Краткое описание

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.

Ключевые слова: lung cancer, A549, lutein, tunnel, DAPI, PI3K/AKT

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