scholarly journals P1‐54: Paclitaxel impedes g1 phase progression in gefitinib‐resistant non‐small‐cell lung cancer

Respirology ◽  
2021 ◽  
Vol 26 (S3) ◽  
pp. 94-94
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
G1 Phase ◽  
Small Cell Lung ◽  
Phase Progression

scholarly journals Lentivirus-mediated knockdown of TSP50 suppresses the growth of non-small cell lung cancer cells via G0/G1 phase arrest

2016 ◽  
Vol 35 (6) ◽  
pp. 3409-3418 ◽  
Author(s):  
WEN-LIANG QIAO ◽  
HAI-YANG HU ◽  
BO-WEN SHI ◽  
LI-JUAN ZANG ◽  
WEI JIN ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
G1 Phase ◽  
Small Cell Lung ◽  
Phase Arrest ◽  
G1 Phase Arrest

scholarly journals Ubiquitin Ligase Cbl-b Is Involved in Icotinib (BPI-2009H)-Induced Apoptosis and G1 Phase Arrest ofEGFRMutation-Positive Non-Small-Cell Lung Cancer

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Xiaodong Mu ◽  
Ye Zhang ◽  
Xiujuan Qu ◽  
Kezuo Hou ◽  
Jian Kang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Ubiquitin Ligase ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
G1 Phase ◽  
Small Cell Lung ◽  
Phase Arrest ◽  
G1 Phase Arrest ◽  
Egfr Mutated

Epidermal growth factor receptor (EGFR) is one of the most promising targets for non-small-cell lung cancer (NSCLC). Icotinib, a highly selective EGFR tyrosine kinase inhibitor (EGFR-TKI), has shown promising clinical efficacy and safety in patients with NSCLC. The exact molecular mechanism of icotinib remains unclear. In this study, we first investigated the antiproliferative effect of icotinib on NSCLC cells. Icotinib significantly inhibited proliferation of the EGFR-mutated lung cancer HCC827 cells. The IC50values at 48 and 72 h were 0.67 and 0.07 μM, respectively. Flow cytometric analysis showed that icotinib caused the G1 phase arrest and increased the rate of apoptosis in HCC827 cells. The levels of cyclin D1 and cyclin A2 were decreased. The apoptotic process was associated with activation of caspase-3, -8, and poly(ADP-ribose) polymerase (PARP). Further study revealed that icotinib inhibited phosphorylation of EGFR, Akt, and extracellular signal-regulated kinase. In addition, icotinib upregulated ubiquitin ligase Cbl-b expression. These observations suggest that icotinib-induced upregulation of Cbl-b is responsible, at least in part, for the antitumor effect of icotinib via the inhibition of phosphoinositide 3-kinase (PI3K)/Akt and mitogen-activated protein kinase pathways in EGFR-mutated NSCLC cells.

scholarly journals Role of FBXW7 in the quiescence of gefitinib-resistant lung cancer stem cells in EGFR-mutant non-small cell lung cancer

2019 ◽  
Author(s):  
Moulid Hidayat ◽  
Yoichiro Mitsuishi ◽  
Fumiyuki Takahashi ◽  
Ken Tajima ◽  
Toshifumi Yae ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
G1 Phase ◽  
Small Cell Lung ◽  
Egfr Mutant

Several recent studies suggest that cancer stem cells (CSCs) are involved in intrinsic resistance to cancer treatment. Maintenance of quiescence is crucial for establishing resistance of CSCs to cancer therapeutics. F-box/WD repeat-containing protein 7 (FBXW7) is a ubiquitin ligase that regulates quiescence by targeting the c-MYC protein for ubiquitination. We previously reported that gefitinib-resistant persisters (GRPs) in EGFR-mutant non-small cell lung cancer (NSCLC) cells highly expressed octamer-binding transcription factor 4 (Oct-4) as well as the lung CSC marker CD133, and they exhibited distinctive features of the CSC phenotype. However, the role of FBXW7 in lung CSCs and their resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors in NSCLC is not fully understood. In this study, we developed GRPs from the two NSCLC cell lines PC9 and HCC827, which express an EGFR exon 19 deletion mutation, by treatment with a high concentration of gefitinib. The GRPs from both PC9 and HCC827 cells expressed high levels of CD133 and FBXW7, but low levels of c-MYC. Cell cycle analysis demonstrated that the majority of GRPs existed in the G0/G1 phase. Knockdown of the FBXW7 gene significantly reduced the cell number of CD133-positive GRPs and reversed the cell population in the G0/G1-phase. We also found that FBXW7 expression in CD133-positive cells was increased and c-MYC expression was decreased in gefitinib-resistant tumors of PC9 cells in mice and in 9 out of 14 tumor specimens from EGFR-mutant NSCLC patients with acquired resistance to gefitinib. These findings suggest that FBXW7 plays a pivotal role in the maintenance of quiescence in gefitinib-resistant lung CSCs in EGFR mutation-positive NSCLC.

scholarly journals CCL21/CCR7 Promotes G2/M Phase Progression via the ERK Pathway in Human Non-Small Cell Lung Cancer Cells

PLoS ONE ◽  
2011 ◽  
Vol 6 (6) ◽  
pp. e21119 ◽  
Author(s):  
Ying Xu ◽  
Lifeng Liu ◽  
Xueshan Qiu ◽  
Lili Jiang ◽  
Bo Huang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Erk Pathway ◽  
Small Cell Lung ◽  
M Phase ◽  
Phase Progression
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