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Sesamin suppresses NSCLC cell proliferation and induces apoptosis via Akt/p53 pathway.
Toxicology and Applied Pharmacology ( IF 3.8 ) Pub Date : 2019-12-03 , DOI: 10.1016/j.taap.2019.114848
Yueming Chen 1 , Huachao Li 1 , Weinan Zhang 1 , Wanchen Qi 1 , Changpeng Lu 1 , Huiliang Huang 1 , Zhicheng Yang 1 , Bing Liu 2 , Luyong Zhang 3
Affiliation  

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with a disappointing prognosis. The aim of this study was to investigate the anticancer effect of sesamin and the underlying mechanism. The MTT assay was used to detect the proliferation of NSCLC cells. The cell cycle and apoptosis were analyzed by flow cytometry. The protein levels of Akt, p-Akt (Ser473), p53, cyclin D1, CDK2, MDM2, p-MDM2 (Ser166) were detected by western blotting. The expression of p-Akt (Ser473), p53 and Ki67 in vivo was analyzed by IHC. Histopathologic analyses of major organs (heart, liver, spleen, lung and kidney) were performed by H&E staining. The results show that sesamin suppressed cell proliferation and induced apoptosis of NSCLC cells (A549 and H1792) in a dose-dependent manner. Treatment with sesamin caused cell cycle arrest at G1 phase and inhibited cyclin D1 and CDK2 expression. In addition, sesamin inhibited Akt activity and upregulated p53 expression both in vivo and in vitro. When Akt and p53 were suppressed by LY294002 and PFTα, respectively, sesamin exerted no additional effects. The in vivo results mostly matched the in vitro findings. Specifically, sesamin exerted little damage to major organs. Taken together, this study demonstrates that sesamin suppresses NSCLC cell proliferation by induction of G1 phase cell cycle arrest and apoptosis via Akt/p53 pathway. Therefore, sesamin may be a promising adjuvant treatment for NSCLC therapy.

中文翻译:

芝麻素通过Akt / p53途径抑制NSCLC细胞增殖并诱导凋亡。

非小细胞肺癌(NSCLC)是最常见的肺癌类型,预后令人失望。这项研究的目的是研究芝麻素的抗癌作用及其潜在机制。使用MTT测定法检测NSCLC细胞的增殖。通过流式细胞仪分析细胞周期和凋亡。通过蛋白质印迹检测Akt,p-Akt(Ser473),p53,细胞周期蛋白D1,CDK2,MDM2,p-MDM2(Ser166)的蛋白水平。通过IHC分析体内p-Akt(Ser473),p53和Ki67的表达。通过H&E染色对主要器官(心脏,肝脏,脾脏,肺和肾脏)进行了组织病理学分析。结果显示芝麻素以剂量依赖性方式抑制NSCLC细胞(A549和H1792)的细胞增殖并诱导其凋亡。芝麻素处理可导致细胞周期停滞在G1期,并抑制细胞周期蛋白D1和CDK2的表达。此外,芝麻素在体内和体外均抑制Akt活性并上调p53表达。当LY294002和PFTα分别抑制Akt和p53时,芝麻素没有其他作用。体内结果大部分与体外发现相符。具体而言,芝麻素对主要器官的损害很小。两者合计,这项研究表明芝麻素通过诱导G1期细胞周期停滞和经由Akt / p53途径的凋亡来抑制NSCLC细胞增殖。因此,芝麻素可能是NSCLC治疗的有希望的辅助治疗方法。当LY294002和PFTα分别抑制Akt和p53时,芝麻素没有其他作用。体内结果大部分与体外发现相符。具体而言,芝麻素对主要器官的损害很小。两者合计,这项研究表明芝麻素通过诱导G1期细胞周期停滞和经由Akt / p53途径的凋亡来抑制NSCLC细胞增殖。因此,芝麻素可能是NSCLC治疗的有希望的辅助治疗方法。当LY294002和PFTα分别抑制Akt和p53时,芝麻素没有其他作用。体内结果大部分与体外发现相符。具体而言,芝麻素对主要器官的损害很小。两者合计,这项研究表明芝麻素通过诱导G1期细胞周期停滞和经由Akt / p53途径的凋亡来抑制NSCLC细胞增殖。因此,芝麻素可能是NSCLC治疗的有希望的辅助治疗方法。
更新日期:2019-12-04
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