scholarly journals Sotetsuflavone Induces Autophagy in Non-Small Cell Lung Cancer Through Blocking PI3K/Akt/mTOR Signaling Pathway in Vivo and in Vitro

2019 ◽  
Vol 10 ◽  
Author(s):  
Shaohui Wang ◽  
Xiaoling Xu ◽  
Yanlan Hu ◽  
Tao Lei ◽  
Tongxiang Liu
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Small Cell Lung

scholarly journals LKB1/AMPK/mTOR Signaling Pathway in Non-small-cell Lung Cancer

2013 ◽  
Vol 14 (7) ◽  
pp. 4033-4039 ◽  
Author(s):  
Dong Han ◽  
Shao-Jun Li ◽  
Yan-Ting Zhu ◽  
Lu Liu ◽  
Man-Xiang Li
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Small Cell Lung

scholarly journals The Potential Role of Cathepsin K in Non-Small Cell Lung Cancer

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4136
Author(s):  
Hui Yang ◽  
Jasmine Heyer ◽  
Hui Zhao ◽  
Shengxian Liang ◽  
Rui Guo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Cathepsin K ◽  
Small Cell ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Small Cell Lung

(1) Background: Cathepsin K has been found overexpressed in several malignant tumors. However, there is little information regarding the involvement of Cathepsin K in non-small cell lung cancer (NSCLC). (2) Methods: Cathepsin K expression was tested in human NSCLC cell lines A549 and human embryo lung fibroblast MRC-5 cells using Western blot and immunofluorescence assay. Cathepsin K was transiently overexpressed or knocked down using transfection with a recombinant plasmid and siRNA, respectively, to test the effects on cell proliferation, migration, invasion, and on the mammalian target of rapamycin (mTOR) signaling pathway. (3) Results: Expression of Cathepsin K was increased significantly in A549 cells and diffused within the cytoplasm compared to the MRC-5 cells used as control. Cathepsin K overexpression promoted the proliferation, migration, and invasion of A549 cells, accompanied by mTOR activation. Cathepsin K knockdown reversed the above malignant behavior and inhibited the mTOR signaling activation, suggesting that Cathepsin K may promote the progression of NSCLC by activating the mTOR signaling pathway. (4) Conclusion: Cathepsin K may potentially represent a viable drug target for NSCLC treatment.

scholarly journals Qiyusanlong Formula Induces Autophagy in Non-Small-Cell Lung Cancer Cells and Xenografts through the mTOR Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yating Gao ◽  
Xinheng Wang ◽  
Qinjun Yang ◽  
Xiaole Wang ◽  
Xingxing Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
A549 Cells ◽  
Small Cell ◽  
Mtor Signaling Pathway ◽  
Small Cell Lung

Objective. Qiyusanlong (QYSL) formula has been used in the clinic for more than 20 years and has been proved to have pronounced efficacy in the treatment of non-small-cell lung cancer (NSCLC). This work aims to evaluate the molecular mechanism of QYSL formula action on NSCLC, specifically in relation to autophagy induction. Methods. In vitro, CCK-8 was used to detect the effect of QYSL serum on cell viability in A549 cells. In vivo, A549 cells were implanted subcutaneously in nude mice to establish a xenograft model. TUNEL staining was used to measure cell apoptosis and TEM to observe the autophagy-related morphological changes in vitro and in vivo. Western blotting, RT-qPCR, and immunofluorescence were used to measure autophagy-related proteins. In addition, rapamycin (an inhibitor of mTOR and inducer of autophagy) and MHY1485 (an activator of mTOR and inhibitor of autophagy) were used to determine whether QYSL-induced autophagy was regulated by the mTOR pathway. Results. QYSL serum inhibited the cell viability of A549 cells in a concentration‐dependent manner. In vivo, the QYSL formula inhibited xenograft growth. The QYSL formula promoted apoptosis in A549 cells and induced autophagosome formation in vitro and in vivo. In addition, the QYSL formula downregulated the expression of mTOR and p62, while it upregulated the expression of ATG-7 and Beclin-1 and increased the LC3-II/LC3-I ratio. QYSL serum inhibited p-mTOR in a similar manner to rapamycin while reducing the activating effects of MHY1485 on p-mTOR. Conclusion. The QYSL formula has anti-lung cancer effects and promotes autophagy through the mTOR signaling pathway.

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