Dioscin-6′-O-acetate inhibits lung cancer cell proliferation via inducing cell cycle arrest and caspase-dependent apoptosis

Phytomedicine ◽  
2019 ◽  
Vol 53 ◽  
pp. 124-133 ◽  
Author(s):  
Xuejiao Li ◽  
Zhuo Qu ◽  
Songsong Jing ◽  
Xia Li ◽  
Chengcheng Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Lung Cancer Cell ◽  
Cycle Arrest

scholarly journals Engineered Bacteriorhodopsin May Induce Lung Cancer Cell Cycle Arrest and Suppress Their Proliferation and Migration

Molecules ◽  
2021 ◽  
Vol 26 (23) ◽  
pp. 7344
Author(s):  
Chui-Wei Wong ◽  
Ling-Ning Ko ◽  
Hung-Jin Huang ◽  
Chii-Shen Yang ◽  
Shan-hui Hsu
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Light Illumination ◽  
Lung Cancer Cell ◽  
Cycle Arrest ◽  
And Migration

Highly expressible bacteriorhodopsin (HEBR) is a light-triggered protein (optogenetic protein) that has seven transmembrane regions with retinal bound as their chromophore to sense light. HEBR has controllable photochemical properties and regulates activity on proton pumping. In this study, we generated HEBR protein and incubated with lung cancer cell lines (A549 and H1299) to evaluate if there was a growth-inhibitory effect with or without light illumination. The data revealed that the HEBR protein suppressed cell proliferation and induced the G0/G1 cell cycle arrest without light illumination. Moreover, the migration abilities of A549 and H1299 cells were reduced by ~17% and ~31% after incubation with HEBR (40 μg/mL) for 4 h. The Snail-1 gene expression level of the A549 cells was significantly downregulated by ~50% after the treatment of HEBR. In addition, HEBR significantly inhibited the gene expression of Sox-2 and Oct-4 in H1299 cells. These results suggested that the HEBR protein may inhibit cell proliferation and cell cycle progression of lung cancer cells, reduce their migration activity, and suppress some stemness-related genes. These findings also suggested the potential of HEBR protein to regulate the growth and migration of tumor cells, which may offer the possibility for an anticancer drug.

scholarly journals TIFA Promotes Cell Survival and Migration in Lung Adenocarcinoma

2018 ◽  
Vol 47 (5) ◽  
pp. 2097-2108 ◽  
Author(s):  
Wanfu Men ◽  
Wenya Li ◽  
Jungang Zhao ◽  
Yu Li
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
Cycle Arrest ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Background/Aims: TNF-α receptor-associated factor (TRAF)-interacting protein with a forkhead-associated (FHA) domain (TIFA) may mediate the impact of TRAF on the development of lung cancer. The current study was conducted to investigate the expression of TIFA in lung adenocarcinoma and its potential role in the regulation of cancer cell proliferation and migration, and its influence on patient survival. Methods: Specimens of lung adenocarcinoma tissues and their adjacent normal lung tissues were obtained from 116 patients who underwent surgical resection of lung cancer. The expression of TIFA in the lung tissues was examined by immunohistochemistry, immunoblotting, and real-time RT-PCR in four different lung cancer cell lines and one normal bronchial epithelial cell line (BEAS-2B). TIFA was silenced by RNAi technique, and cell proliferation was then assessed by the CCK8 method. Furthermore, cell migration was determined by wound-healing trans-well and wound-healing migration assays. Additionally, cell-cycle arrest and apoptosis were assessed by flow cytometry analysis. Results: TIFA was positively detected in 63 (54.3%) out of 116 lung adenocarcinoma specimens, which was significantly higher than the respective rate established in normal tissues adjacent to the tumor (30.1%, p < 0.05). The overall survival rate was significantly lower in the patients with positive TIFA expression than that in the patients with negative TIFA expression (p < 0.05). TIFA was also highly expressed in the lung cancer cell lines (H1299, H1975, and HCC827) tested. It is noteworthy that siRNA suppressed the expression of TIFA, which contributed to the attenuation of cell proliferation and migration, but promoted cell-cycle arrest and apoptosis. Furthermore, the silencing of TIFA caused upregulation of p53, p21, and cleaved-caspase-3, but downregulation of Bcl-2, cyclin D1, and CDK4, as well as phosphorylation of IKKß, IκB, and p65. Conclusions: TIFA may serve as a biomarker in the prediction of lung adenocarcinoma. Furthermore, TIFA may modulate lung cancer cell survival and proliferation through regulating the synthesis of apoptosis-associated proteins.

Molecular imaging of p53 signal pathway in lung cancer cell cycle arrest induced by cisplatin

2012 ◽  
Vol 52 (11) ◽  
pp. 900-907 ◽  
Author(s):  
Shenxu Wang ◽  
Weijie Li ◽  
Zengfu Xue ◽  
Yuanyuan Lu ◽  
Kazim Narsinh ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Molecular Imaging ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Signal Pathway ◽  
Lung Cancer Cell ◽  
Cycle Arrest
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