scholarly journals CEP131 knockdown inhibits cell proliferation by inhibiting the ERK and AKT signaling pathways in non‑small cell lung cancer

2020 ◽  
Author(s):  
Junying Wang ◽  
Xiaoping Yang ◽  
Shixin Han ◽  
Lizhi Zhang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Signaling Pathways ◽  
Cell Lung Cancer ◽  
Akt Signaling ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals Cordycepin Reverses Cisplatin Resistance in Non-small Cell Lung Cancer by Activating AMPK and Inhibiting AKT Signaling Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Xiao-Zhong Liao ◽  
Ying Gao ◽  
Hong-Wei Zhao ◽  
Mi Zhou ◽  
Dan-Lei Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Signaling Pathways ◽  
Cell Lung Cancer ◽  
Akt Signaling ◽  
Small Cell ◽  
Akt Pathway ◽  
Small Cell Lung ◽  
Proliferation And Apoptosis

Cisplatin (DDP) is the first-line chemotherapeutic agent against lung cancer. However, the therapeutic effect of DDP loses over time due to the acquired drug resistance in non-small cell lung cancer (NSCLC) cells. In recent years, the role of the traditional Chinese medicine (TCM) cordycepin (Cor) in cancer treatment has been attracting attention. However, the effects of Cor on DDP resistance in NSCLC are unclear. In the present study, we aimed to investigate the effects of Cor in combination with DDP on cell proliferation and apoptosis in NSCLC and explore possible underlying mechanisms. The cell proliferation and apoptosis were analyzed in NSCLC parental (A549) and DDP-resistant (A549DDP) cells treated with DDP alone or in combination with Cor both in vitro and in vivo. Different genes and signaling pathways were investigated between DDP-sensitive and DDP-resistant A549 cells by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. The perturbations of the MAPK and PI3K-AKT signaling pathways were evaluated by Western blot analysis. Our data showed that Cor markedly enhanced DDP inhibition on cell proliferation and promotion of apoptosis compared to the DDP-alone group in both A549 and A549DDP cells. The synergic actions were associated with activation of AMPK; inhibition of AKT, mTOR, and downstream P709S6K; and S6 phosphorylation in the AKT pathway compared with DDP alone. Collectively, combination of Cor and DDP has a synergistic effect in inhibiting proliferation and promoting apoptosis of NSCLC cells in the presence or absence of DDP resistance. The antitumor activity is associated with activation of AMPK and inhibition of the AKT pathway to enhance DDP inhibition on NSCLC. Our results suggested that Cor in combination with DDP could be an additional therapeutic option for the treatment of DDP-resistant NSCLC.

scholarly journals Delphinidin Reduces Cell Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Targeting EGFR/VEGFR2 Signaling Pathways

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e77270 ◽  
Author(s):  
Harish Chandra Pal ◽  
Samriti Sharma ◽  
Leah Ray Strickland ◽  
Jyoti Agarwal ◽  
Mohammad Athar ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Vegfr2 Signaling

scholarly journals VASH2 Promotes Cell Proliferation and Resistance to Doxorubicin in Non-Small Cell Lung Cancer via AKT Signaling

2020 ◽  
Vol 28 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Xiangbin Tan ◽  
Zefei Liao ◽  
Shuangyou Zou ◽  
Liangyun Ma ◽  
Aimin Wang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Akt Signaling ◽  
Small Cell ◽  
Nsclc Cell ◽  
Small Cell Lung ◽  
P Glycoprotein ◽  
Resistance To Doxorubicin

Vasohibin2 (VASH2), a proangiogenic factor, has been demonstrated to play an oncogenic role in some common human cancers. However, the detailed function of VASH2 in non-small cell lung cancer (NSCLC) has not previously been studied. In this study, we found that VASH2 was significantly upregulated in NSCLC tissues and cell lines, and its increased expression was associated with NSCLC progression and poor prognosis of patients. Knockdown of VASH2 markedly inhibited cell proliferation and P-glycoprotein expression in NSCLC cells. Overexpression of VASH2 enhanced cell proliferation, P-glycoprotein expression, as well as doxorubicin resistance in NSCLC cells. Moreover, the expression levels of VASH2 were significantly increased in newly established doxorubicin-resistant NSCLC cells. Molecular mechanism investigation revealed that inhibition of VASH2 expression in NSCLC cells suppressed the activity of AKT signaling, and overexpression of VASH2 enhanced the activity of AKT signaling. We further showed that downregulation of AKT signaling activity using AKT inhibitor LY294002 markedly inhibited NSCLC cell proliferation and resistance to doxorubicin induced by VASH2. In conclusion, the findings in the present study indicate that VASH2 promotes NSCLC cell proliferation and resistance to doxorubicin via modulation of AKT signaling. Thus, we suggest that VASH2 may become a potential therapeutic target for the treatment of NSCLC.

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