Potential chemotherapeutic effect of betalain against human non‐small cell lung cancer through PI3K /Akt/ mTOR signaling pathway

(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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Effect of microRNA-145 on proliferation and apoptosis of human non-small cell lung cancer A549 cells by regulating mTOR signaling pathway

Journal of Cellular Biochemistry ◽

10.1002/jcb.26629 ◽

2017 ◽

Cited By ~ 8

Author(s):

Jian-Cheng Li ◽

Jun-Qiong Zheng

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Signaling Pathway ◽

Cell Lung Cancer ◽

A549 Cells ◽

Small Cell ◽

Mtor Signaling ◽

Mtor Signaling Pathway ◽

Small Cell Lung ◽

Proliferation And Apoptosis

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Interleukin 7 Inhibit Autophagy via P53 Regulated AMPK/mTOR Signaling Pathway in Non-small Cell Lung Cancer

10.21203/rs.3.rs-750367/v1 ◽

2021 ◽

Author(s):

Yunjia Zhu ◽

Xi Jiang ◽

Zhiying Ding ◽

Jian Ming

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Signaling Pathway ◽

Cell Lung Cancer ◽

Tumor Stage ◽

Small Cell ◽

Mtor Signaling ◽

Mtor Signaling Pathway ◽

Small Cell Lung ◽

Interleukin 7

Abstract Interleukin 7(IL-7) has been demonstrated regulating lymphangiogenesis, apoptosis, and proliferation. Whether IL-7 induce or inhibit autophagy in non-small cell lung cancer(NSCLC) are unknown. Methods In this study, Western blot was used to detect cytoplasmic and nuclear protein of p53, total protein of AMP-activated protein kinase(AMPK) and mammalian target of rapamycin (mTOR). Quantitative Real-Time PCR(qRT-PCR) was used to detect p53 mRNA level after treated with IL-7. Then using transmission electron microscopy (TEM) to observe the morphological change of autophagosome. 123 cases of NSCLC were collected for survival analysis, immunohistochemistry staining and cox regression multivariate analysis. Results We find that IL-7 induce the p53 translocation from nucleus to cytoplasm, then IL-7 down-regulate phosphorylation of AMPK and up-regulate phosphorylation of mTOR. The expression of AMPK and p53 were associated with IL-7/IL-7R and mTOR expression. Clinically, AMPK and p53 were well correlated with stage and survival of lung cancer patients. IL-7R, mTOR and tumor stage were the strongest predictors of survival. Conclusion In conclusion, IL-7 inhibit autophagy in NSCLC via P53 regulated AMPK/mTOR signaling pathway. AMPK and p53 are correlated with patients’ survival. IL-7R, mTOR and tumor stage are the strongest predictor of survival.

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