Roles of MKK1/2-ERK1/2 and Phosphoinositide 3-Kinase–AKT Signaling Pathways in Erlotinib-Induced Rad51 Suppression and Cytotoxicity in Human Non–Small Cell Lung Cancer Cells

2009 ◽  
Vol 7 (8) ◽  
pp. 1378-1389 ◽  
Author(s):  
Jen-Chung Ko ◽  
Shih-Ci Ciou ◽  
Jhih-Yuan Jhan ◽  
Chao-Min Cheng ◽  
Ying-Jhen Su ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cell Lung Cancer ◽  
Akt Signaling ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Phosphoinositide 3 Kinase

scholarly journals Gelsolin Promotes Radioresistance in Non–Small Cell Lung Cancer Cells Through Activation of Phosphoinositide 3-Kinase/Akt Signaling

2016 ◽  
Vol 16 (4) ◽  
pp. 512-518 ◽  
Author(s):  
Ru-Sen Zhao ◽  
Wei Wang ◽  
Jun-Ping Li ◽  
Chun-Mei Liu ◽  
Liya He
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Akt Signaling ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
H460 Cells ◽  
Phosphoinositide 3 Kinase

Gelsolin is an actin-binding protein and acts as an important regulator of cell survival. This study aimed to determine the function of gelsolin in the radioresistance of non–small cell lung cancer cells. We examined the expression of gelsolin in radioresistant A549 and H460 cells and their parental cells. The effects of gelsolin overexpression and knockdown on the clonogenic survival and apoptosis of non–small cell lung cancer cells after irradiation were studied. The involvement of phosphoinositide 3-kinase/Akt signaling in the action of gelsolin was checked. We found that gelsolin was significantly upregulated in radioresistant A549 and H460 cells. Overexpression of gelsolin significantly ( P < .05) increased the number of colonies from irradiated A549 and H460 cells compared to transfection of empty vector. In contrast, knockdown of gelsolin significantly ( P < .05) suppressed colony formation after irradiation. Gelsolin-overexpressing cells displayed reduced apoptosis in response to irradiation, which was coupled with decreased levels of cleaved caspase-3 and poly adenosine diphosphate-ribose polymerase. Ectopic expression of gelsolin significantly ( P < .05) enhanced the phosphorylation of Akt compared to nontransfected cells. Pretreatment with the phosphoinositide 3-kinase inhibitor LY294002 (20 μmol/L) significantly decreased clonogenic survival and enhanced apoptosis in gelsolin-overexpressing A549 and H460 cells after irradiation. Taken together, gelsolin upregulation promotes radioresistance in non–small cell lung cancer cells, at least partially, through activation of phosphoinositide 3-kinase/Akt signaling.

scholarly journals ZNF259 inhibits non-small cell lung cancer cells proliferation and invasion by FAK-AKT signaling

2017 ◽  
Vol Volume 9 ◽  
pp. 879-889 ◽  
Author(s):  
Yuemei Shan ◽  
Wei Cao ◽  
Tao Wang ◽  
Guiyang Jiang ◽  
Yong Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Akt Signaling ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Proliferation And Invasion

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 Effects of Apatinib on the “Stemness” of Non-Small-Cell Lung Cancer Cells In Vivo and Its Related Mechanisms

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Bin Yang ◽  
Yan Wang ◽  
Zhuoying Chen ◽  
Yi-Ming Feng ◽  
Liang-Liang Shi
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Control Group ◽  
Small Cell Lung

Objective. To investigate the effects of Apatinib on the “stemness” of lung cancer cells in vivo and to explore its related mechanisms. Methods. A xenograft model of lung cancer cells A549 was established in nude mice and randomized into a control group (n = 4) and an Apatinib group (n = 4). Tumor tissues were harvested after 2 weeks, and mRNA was extracted to detect changes in stemness-related genes (CD133, EPCAM, CD13, CD90, ALDH1, CD44, CD45, SOX2, NANOG, and OCT4) and Wnt/β-catenin, Hedgehog, and Hippo signal pathways. Results. Compared with the control group, the volume and weight of nude mice treated with Apatinib were different and had statistical significance. Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3. Apatinib treatment also inhibited the Wnt/β-catenin, Hedgehog, and Hippo signaling pathways. Conclusion. Apatinib suppressed the growth of non-small-cell lung cancer cells by repressing the stemness of lung cancer through the inhibition of the Hedgehog, Hippo, and Wnt signaling pathways.

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