Curcumin potentiates the galbanic acid-induced anti-tumor effect in non-small cell lung cancer cells through inhibiting Akt/mTOR signaling pathway

Life Sciences ◽  
2019 ◽  
Vol 239 ◽  
pp. 117044 ◽  
Author(s):  
Qian Zhang ◽  
Haowen Qiao ◽  
Dedong Wu ◽  
Hui Lu ◽  
Liying Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Small Cell Lung ◽  
Galbanic Acid

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.

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