scholarly journals Detection of microRNA-200b may predict the inhibitory effect of gefitinib on non-small cell lung cancer and its potential mechanism

2016 ◽  
Vol 12 (6) ◽  
pp. 5349-5355 ◽  
Author(s):  
Zhiwu Liu ◽  
Liqiong Yao ◽  
Bangyun Tan ◽  
Li Li ◽  
Baojin Chen
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Inhibitory Effect ◽  
Small Cell ◽  
Potential Mechanism ◽  
Small Cell Lung

scholarly journals Therapeutic effects of the novel Leucyl-tRNA synthetase inhibitor BC-LI-0186 in non-small cell lung cancer

2019 ◽  
Vol 11 ◽  
pp. 175883591984679 ◽  
Author(s):  
Eun Young Kim ◽  
Jin Gu Lee ◽  
Jung Mo Lee ◽  
Arum Kim ◽  
Hee Chan Yoo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Antitumor Effect ◽  
Inhibitory Effect ◽  
Trna Synthetase ◽  
Small Cell ◽  
Therapeutic Effects ◽  
Small Cell Lung

Objective: Leucyl-tRNA synthetase (LRS) is an aminoacyl-tRNA synthetase catalyzing ligation of leucine to its cognate tRNA and is involved in the activation of mTORC1 by sensing cytoplasmic leucine. In this study, the usefulness of LRS as a therapeutic target of non-small cell lung cancer (NSCLC) and the anticancer effect of the LRS inhibitor, BC-LI-0186, was evaluated. Methods: LRS expression and the antitumor effect of BC-LI-0186 were evaluated by immunohistochemical staining, immunoblotting, and live cell imaging. The in vivo antitumor effect of BC-LI-0186 was evaluated using Lox-Stop-Lox (LSL) K-ras G12D mice. Results: LRS was frequently overexpressed in NSCLC tissues, and its expression was positively correlated with mTORC1 activity. The guanosine-5’-triphosphate (GTP) binding status of RagB was related to the expression of LRS and the S6K phosphorylation. siRNA against LRS inhibited leucine-mediated mTORC1 activation and cell growth. BC-LI-0186 selectively inhibited phosphorylation of S6K without affecting phosphorylation of AKT and leucine-mediated co-localization of Raptor and LAMP2 in the lysosome. BC-LI-0186 induced cleaved poly (ADP-ribose) polymerase (PARP) and caspase-3 and increase of p62 expression, showing that it has the autophagy-inducing property. BC-LI-0186 has the cytotoxic effect at nanomolar concentration and its GI50 value was negatively correlated with the degree of LRS expression. BC-LI-0186 showed the antitumor effect, which was comparable with that of cisplatin, and mTORC1 inhibitory effect in a lung cancer model. Conclusions: BC-LI-0186 inhibits the noncanonical mTORC1-activating function of LRS. These results provide a new therapeutic strategy for NSCLC and warrant future clinical development by targeting LRS.

Inhibitory effect of riccardin D on growth of human non-small cell lung cancer: In vitro and in vivo studies

Lung Cancer ◽  
2012 ◽  
Vol 76 (3) ◽  
pp. 300-308 ◽  
Author(s):  
Xia Xue ◽  
De-Fu Sun ◽  
Cui-Cui Sun ◽  
Hui-Ping Liu ◽  
Bin Yue ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Inhibitory Effect ◽  
Small Cell ◽  
In Vivo Studies ◽  
Small Cell Lung

scholarly journals Re-188 Enhances the Inhibitory Effect of Bevacizumab in Non-Small-Cell Lung Cancer

Molecules ◽  
2016 ◽  
Vol 21 (10) ◽  
pp. 1308 ◽  
Author(s):  
Jie Xiao ◽  
Xiaobo Xu ◽  
Xiao Li ◽  
Yanli Li ◽  
Guobing Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Inhibitory Effect ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals Triptolide suppresses the growth and metastasis of non-small cell lung cancer by inhibiting β-catenin-mediated epithelial–mesenchymal transition

2021 ◽  
Author(s):  
Qiu-di Deng ◽  
Xue-ping Lei ◽  
Yi-hang Zhong ◽  
Min-shan Chen ◽  
Yuan-yu Ke ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Inhibitory Effect ◽  
Small Cell ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Small Cell Lung ◽  
Mesenchymal Transition

AbstractNon-small cell lung cancer (NSCLC) is characterized by a high incidence of metastasis and poor survival. As epithelial–mesenchymal transition (EMT) is well recognized as a major factor initiating tumor metastasis, developing EMT inhibitor could be a feasible treatment for metastatic NSCLC. Recent studies show that triptolide isolated from Tripterygium wilfordii Hook F attenuated the migration and invasion of breast cancer, colon carcinoma, and ovarian cancer cells, and EMT played important roles in this process. In the present study we investigated the effect of triptolide on the migration and invasion of NSCLC cell lines. We showed that triptolide (0.5, 1.0, 2.0 nM) concentration-dependently inhibited the migration and invasion of NCI-H1299 cells. Triptolide treatment concentration-dependently suppressed EMT in NCI-H1299 cells, evidenced by significantly elevated E-cadherin expression and reduced expression of ZEB1, vimentin, and slug. Furthermore, triptolide treatment suppressed β-catenin expression in NCI-H1299 and NCI-H460 cells, overexpression of β-catenin antagonized triptolide-caused inhibition on EMT, whereas knockout of β-catenin enhanced the inhibitory effect of triptolide on EMT. Administration of triptolide (0.75, 1.5 mg/kg per day, ip, every 2 days) for 18 days in NCI-H1299 xenograft mice dose-dependently suppressed the tumor growth, restrained EMT, and decreased lung metastasis, as evidence by significantly decreased expression of mesenchymal markers, increased expression of epithelial markers as well as reduced number of pulmonary lung metastatic foci. These results demonstrate that triptolide suppresses NSCLC metastasis by targeting EMT via reducing β-catenin expression. Our study implies that triptolide may be developed as a potential agent for the therapy of NSCLC metastasis.

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