Wnt Signaling in Stem Cells and Lung Cancer

2007 ◽  
pp. 27-58 ◽  
Author(s):  
B. He ◽  
D. M. Jablons
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Wnt Signaling

scholarly journals Nutlin-3-Induced Sensitization of Non-Small Cell Lung Cancer Stem Cells to Axitinib-Induced Apoptosis Through Repression of Akt1/Wnt Signaling

2019 ◽  
Vol 27 (9) ◽  
pp. 987-995
Author(s):  
Meng Wang ◽  
Xin Wang ◽  
Yuan Li ◽  
Qiang Xiao ◽  
Xiao-Hai Cui ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cell Division ◽  
Small Cell Lung Cancer ◽  
Wnt Signaling ◽  
Small Cell ◽  
Small Cell Lung ◽  
P53 Expression ◽  
Induction Of Apoptosis ◽  
Induced Apoptosis

The aim of this study was to investigate the potential biological activities of nutlin-3 in the regulation of growth and proliferation of non-small cell lung cancer (NSCLC) stem cells (CSCs), which may help in sensitizing to axitinib-induced apoptosis. Nutlin-3 induction of p53 expression was used to test its role in controlling the cell division pattern and apoptosis of NSCLC cells. A549 cells and H460 cells were pretreated with nutlin-3 and then treated with either an Akt1 activator or shRNA-GSK3β, to investigate the potential role of p53 sensitization in the biological effects of axitinib. We also determined the expression levels of GSK3β and p-Akt1 in patients with NSCLC and determined their potential association with survival data using Kaplan‐Meier plots and CBIOTAL. Increased p53 expression stimulated the induction of apoptosis by axitinib and promoted asymmetric cell division (ACD) of NSCLC CSCs. The repression of Akt phosphorylation induced by nutlin-3 promoted the ACD of lung CSCs, decreasing the proportion of the stem cell population. In addition to the induction of apoptosis by axitinib through inhibition of Wnt signaling, nutlin-3 treatment further enhanced axitinib-induced apoptosis by inhibiting Akt1/GSK3β/Wnt signaling. The low expression of GSK3β and increased expression of p-Akt in patients with NSCLC were closely associated with the development of NSCLC. TP53 stimulates the induction of apoptosis in NSCLC by axitinib and the ACD of lung CSCs through its regulatory effects on the p53/Akt/GSK3β pathways.

Wnt Signaling in Stem Cells and Non–Small-Cell Lung Cancer

2005 ◽  
Vol 7 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Biao He ◽  
Richard N. Barg ◽  
Liang You ◽  
Zhidong Xu ◽  
Noemi Reguart ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Small Cell Lung Cancer ◽  
Wnt Signaling ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals Wnt5a Increases Properties of Lung Cancer Stem Cells and Resistance to Cisplatin through Activation of Wnt5a/PKC Signaling Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Jiali Yang ◽  
Kangjian Zhang ◽  
Jing Wu ◽  
Juan Shi ◽  
Jing Xue ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
A549 Cells ◽  
Pkc Signaling ◽  
Lung Cancer Stem Cells ◽  
Nsclc Patients

The development of chemoresistance to cisplatin regimens causes a poor prognosis in patients with advanced NSCLC. The role of noncanonical Wnt signaling in the regulation of properties of lung cancer stem cells and chemoresistance was interrogated, by accessing capacities of cell proliferation, migration, invasion, and clonogenicity as well as the apoptosis in A549 cell lines and cisplatin-resistant A549 cells treated with Wnt5a conditional medium or protein kinase C (PKC) inhibitor GF109203X. Results showed that the noncanonical Wnt signaling ligand, Wnt5a, could promote the proliferation, migration, invasion, and colony formation in A549 lung adenocarcinoma cells and cisplatin-resistant A549/DDP cells and increase the fraction of ALDH-positive cell in A549/DDP cells. An exposure of cells to Wnt5a led to a significant reduction of A549/DDP cell apoptosis but not A549 cells. An addition of GF109203X could both strikingly increase the baseline apoptosis and resensitize the Wnt5a-inhibited cell apoptosis. Interestingly, an inhibition of Wnt/PKC signaling pathway could reduce properties of lung cancer stem cells, promote cell apoptosis, and resensitize cisplatin-resistant cells to cisplatin via a caspase/AIF-dependent pathway. These data thus suggested that the Wnt5a could promote lung cancer cell mobility and cisplatin-resistance through a Wnt/PKC signaling pathway and a blockage of this signaling may be an alternative therapeutic strategy for NSCLC patients with resistance to chemotherapies.

Wnt signaling regulates the stemness of lung cancer stem cells and its inhibitors exert anticancer effect on lung cancer SPC-A1 cells

2015 ◽  
Vol 32 (4) ◽  
Author(s):  
Xueyan Zhang ◽  
Yuqing Lou ◽  
Huimin Wang ◽  
Xiaoxuan Zheng ◽  
Qianggang Dong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Wnt Signaling ◽  
Anticancer Effect ◽  
Lung Cancer Stem Cells

Stem cells fend off lung cancer

Nature ◽  
2006 ◽  
Author(s):  
Charlotte Schubert
Keyword(s):  
Lung Cancer ◽  
Stem Cells

LIFE SPAN PREDICTION AT METASTATIC NON-SMALL CELL LUNG CANCER

2018 ◽  
Vol 64 (4) ◽  
pp. 522-527
Author(s):  
Aleksey Shutko ◽  
Viktor Mus
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Small Cell Lung Cancer ◽  
Life Span ◽  
Cell Lung Cancer ◽  
Poor Prognosis ◽  
Small Cell ◽  
Hemopoietic Stem Cells ◽  
Small Cell Lung ◽  
Individual Life

Individual parameters of circulating hemopoietic stem cells (HSC) lymphoid origin were measured by cytofluorometry before treatment of patients with metastatic non-small cell lung cancer and were retrospectively compared with individual life span's (LS). The possibility of poor prognosis of treatment's results (LS

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