Abstract
(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.
Highlights
Non-small cell lung cancer (NSCLC) is the leading cause of cancer death among men and women worldwide, with an incidence rate of 1.3 million cases per year [1]
Our findings indicate that Cathepsin K has the significantly reduced the phosphorylation of mammalian target of rapamycin (mTOR) at S2448 in Caki cells [25]
For expression of Cathepsin K has been observed in primary melanoma and melanoma metastases [29]
Summary
Non-small cell lung cancer (NSCLC) is the leading cause of cancer death among men and women worldwide, with an incidence rate of 1.3 million cases per year [1]. Pathway plays important role in maintaining cell growth, proliferation, motility, proliferation, migration, and invasion in vitro. The mTOR signaling with increased p-mTOR expression in up to 90% of patients with adenocarcinoma, 60% of patients with pathway plays an important role in maintaining cell growth, proliferation, motility, and survival [19]. 40% of patients with squamous tumor cell carcinoma mTORcells to been widely studied and employed in order to suppress growth and sensitize activation may be associated with poor prognosis in early. Previous studies have demonstrated that inhibition of Cathepsin K can significantly have widely studiedof and employed clinically in order suppress tumorCathepsin growth andKsensitize reduced thebeen phosphorylation at S2448 in Caki cells to [25]. Previous studies have demonstrated that inhibition of Cathepsin K can activation of the mTOR signaling pathway in NSCLC. Cathepsin K has the potential in developing as a therapeutic target for NSCLC
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