scholarly journals Wnt signaling pathway pharmacogenetics in non-small cell lung cancer

2014 ◽  
Vol 14 (6) ◽  
pp. 509-522 ◽  
Author(s):  
D J Stewart ◽  
D W Chang ◽  
Y Ye ◽  
M Spitz ◽  
C Lu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Wnt Signaling Pathway ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals MicroRNA-520a Suppresses Pathogenesis and Progression of Non-Small-Cell Lung Cancer through Targeting the RRM2/Wnt Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yi Xie ◽  
Congyu Xue ◽  
Shuai Guo ◽  
Lei Yang
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Wnt Signaling Pathway ◽  
Small Cell ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Aberrant Expression ◽  
Normal Tissues

MicroRNAs (miRNAs) regulate multiple cellular behaviors, and their aberrant expression is frequently associated with disease progression. This research focused on the effects of miR-520a on the development of non-small-cell lung cancer (NSCLC) and the molecules involved. Tumor and normal tissues from 24 patients with NSCLC were collected. Differentially expressed miRNAs between tumor tissues and normal tissues were screened using microarrays, and miR-520a was screened to be significantly poorly expressed in tumor samples. Artificial upregulation of miR-520a reduced proliferation, migration and invasion, and resistance to death of NSCLC A549 and H460 cells according to the MTT, EdU labeling, transwell, and flow cytometry assays, respectively. miR-520a upregulation suppressed growth and metastasis of xenograft tumors in vivo. The integrated bioinformatic analysis and dual luciferase assays suggested that miR-520a targeted ribonucleotide reductase subunit 2 (RRM2) mRNA and inactivated the Wnt/β-catenin signaling pathway in NSCLC cells. Upregulation of RRM2 enhanced the malignant behaviors of NSCLCs, but the oncogenic effects of RRM2 were blocked upon miR-520a overexpression. To conclude, this study evidenced that miR-520a inhibits NSCLC progression through suppressing RRM2 and the Wnt signaling pathway. This paper may offer novel insights into NSCLC treatment.

PYGB facilitates cell proliferation and invasiveness in non-small cell lung cancer by activating the Wnt–β-catenin signaling pathway

2020 ◽  
Vol 98 (5) ◽  
pp. 565-574 ◽  
Author(s):  
Lina Xiao ◽  
Wei Wang ◽  
Qiuqiang Huangfu ◽  
Hongjie Tao ◽  
Jingyi Zhang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Wnt Signaling Pathway ◽  
Positive Lymph Node ◽  
Small Cell ◽  
Small Cell Lung

Brain-type glycogen phosphorylase (PYGB) has been correlated with the progression of various human malignancies; however, its effects and regulatory mechanisms in non-small cell lung cancer (NSCLC) are still unclear. We used Western blotting, immunohistochemistry, and qRT-PCR to verify that the protein and mRNA expression levels of PYGB are up-regulated in both NSCLC cell lines and tissues. The expression of PYGB was positively related to TNM stage, positive lymph node metastasis, and poor prognosis in patients with NSCLC. Moreover, overexpression of PYGB promoted cell proliferation, migration, and invasiveness, but inhibited apoptosis, in vitro. Immunofluorescence assays showed that overexpression of PYGB promoted the nuclear import and accumulation of β-catenin. By comparison, silencing PYGB produced the opposite effects. Further, overexpression of PYGB resulted in activation of the Wnt signaling pathway, and transfection with Sh-PYGB produced the opposite effect, and these effects were abrogated by XAV-939 (a β-catenin inhibitor) or overexpression of β-catenin, respectively. Finally, knockdown of PYGB inhibited tumor growth in a mouse model of xenograft tumors. These findings highlight the role of PYGB in the progression of NSCLC, and reveal a link between PYGB and the Wnt–β-catenin signaling pathway, thus providing a new potential target for treatment of NSCLC.

Phanginin R Induces Cytoprotective Autophagy via JNK/c-Jun Signaling Pathway in Non-Small Cell Lung Cancer A549 Cells

2020 ◽  
Vol 20 (8) ◽  
pp. 982-988 ◽  
Author(s):  
Le-Le Zhang ◽  
Han Bao ◽  
Yu-Lian Xu ◽  
Xiao-Ming Jiang ◽  
Wei Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Biological Activities ◽  
A549 Cells ◽  
Immunofluorescence Assay ◽  
Small Cell ◽  
Autophagic Flux ◽  
Small Cell Lung

Background: Cassane-type diterpenoids are widely distributed in the medical plants of genus Caesalpinia. To date, plenty of cassane diterpenoids have been isolated from the genus Caesalpinia, and some of them were documented to exhibit multiple biological activities. However, the effects of these compounds on autophagy have never been reported. Objective: To investigate the effects and mechanisms of the cassane diterpenoids including Phanginin R (PR) on autophagy in Non-Small Cell Lung Cancer (NSCLC) A549 cells. Methods: Western blot analysis and immunofluorescence assay were performed to investigate the effects of the compounds on autophagic flux in A549 cells. The pathway inhibitor and siRNA interference were used to investigate the mechanism of PR. MTT assay was performed to detect cell viability. Results: PR treatment upregulated the expression of phosphatidylethanolamine-modified microtubule-associated protein Light-Chain 3 (LC3-II) in A549 cells. Immunofluorescence assay showed that PR treatment increased the production of red-fluorescent puncta in mRFP-GFP-LC3 plasmid-transfected cells, indicating PR promoted autophagic flux in A549 cells. PR treatment activated the c-Jun N-terminal Kinase (JNK) signaling pathway while it did not affect the classical Akt/mammalian Target of Rapamycin (mTOR) pathway. Pretreatment with the JNK inhibitor SP600125 or siRNA targeting JNK or c-Jun suppressed PR-induced autophagy. In addition, cotreatment with the autophagy inhibitor Chloroquine (CQ) or inhibition of the JNK/c-Jun signaling pathway increased PR-induced cytotoxicity. Conclusion: PR induced cytoprotective autophagy in NSCLC A549 cells via the JNK/c-Jun signaling pathway, and autophagy inhibition could further improve the anti-cancer potential of PR.

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