Li Xin, Wang Dan, Zhao Qing Chun, Shi Tao, Chen Jun
Department of Lung Cancer Surgery, Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Heping District, Tianjin, China.
Department of Lung Cancer Surgery, Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Heping District, Tianjin, China.
Am J Med Sci. 2016 Nov;352(5):524-530. doi: 10.1016/j.amjms.2016.08.027. Epub 2016 Sep 22.
Resveratrol has demonstrated many beneficial effects against cancers; however, the mechanism remains unclear. Non-small cell lung cancer accounts for 80% of lung cancers. The present study was designed to observe the effects and related mechanisms of resveratrol on non-small cell lung cancer in in vitro A549 cells.
The anticancer effects of resveratrol were analyzed on cell viability, migration and invasion, proliferation and apoptosis. Cell viability was determined by sulphorhodamine B assays. Cell proliferation and apoptosis were determined by flow cytometry and migration and invasion by transwell chamber analysis. Expression of STAT-3 was examined by real-time polymerase chain reaction and western blot. Overexpressing vector of STAT-3 was also constructed and transfected into A549 cells to observe the effects of resveratrol on STAT-3 signaling.
The results showed that resveratrol displayed a dose-dependent and time-dependent cytotoxicity action on A549 cell viability. Resveratrol also inhibited proliferation, migration and invasion and promoted apoptosis in a time-dependent manner from 0-72 hours. Further study showed that resveratrol inhibited the messenger RNA and protein expression of STAT-3, and overexpressed STAT-3 abolished the effects of resveratrol on proliferation, apoptosis, migration and invasion totally or in part.
These results suggest that the anticancer effects of resveratrol are mediated by STAT-3 signaling.
白藜芦醇已显示出对癌症有许多有益作用;然而,其机制仍不清楚。非小细胞肺癌占肺癌的80%。本研究旨在观察白藜芦醇对体外培养的A549细胞中非小细胞肺癌的影响及相关机制。
分析白藜芦醇对细胞活力、迁移、侵袭、增殖和凋亡的抗癌作用。通过磺酰罗丹明B法测定细胞活力。通过流式细胞术测定细胞增殖和凋亡,通过Transwell小室分析测定迁移和侵袭。通过实时聚合酶链反应和蛋白质印迹法检测STAT-3的表达。还构建了STAT-3的过表达载体并转染到A549细胞中,以观察白藜芦醇对STAT-3信号传导的影响。
结果表明,白藜芦醇对A549细胞活力表现出剂量依赖性和时间依赖性的细胞毒性作用。白藜芦醇还在0至72小时内以时间依赖性方式抑制增殖、迁移和侵袭,并促进凋亡。进一步研究表明,白藜芦醇抑制STAT-3的信使核糖核酸和蛋白质表达,而过表达的STAT-3完全或部分消除了白藜芦醇对增殖、凋亡、迁移和侵袭的影响。
这些结果表明,白藜芦醇的抗癌作用是由STAT-3信号传导介导的。