scholarly journals TIP30 overcomes gefitinib resistance by regulating cytoplasmic and nuclear EGFR signaling in non‐small cell lung cancer

2021 ◽  
Author(s):  
Shuai Shuai ◽  
Xueyang Liao ◽  
Haixia Wang ◽  
Lusha Liu ◽  
Shiqi Mei ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Egfr Signaling ◽  
Small Cell Lung ◽  
Gefitinib Resistance

scholarly journals The regulation of Neuropilin 1 expression by miR‐338‐3p promotes non‐small cell lung cancer via changes in EGFR signaling

2019 ◽  
Vol 58 (6) ◽  
pp. 1019-1032 ◽  
Author(s):  
Zongli Ding ◽  
Jianjie Zhu ◽  
Yuanyuan Zeng ◽  
Wenwen Du ◽  
Yang Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Egfr Signaling ◽  
Small Cell Lung ◽  
Neuropilin 1

scholarly journals ERK inhibition represses gefitinib resistance in non-small cell lung cancer cells

Oncotarget ◽  
2018 ◽  
Vol 9 (15) ◽  
pp. 12020-12034 ◽  
Author(s):  
Mengfan Qi ◽  
Ye Tian ◽  
Wang Li ◽  
Dan Li ◽  
Tian Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Erk Inhibition ◽  
Gefitinib Resistance

scholarly journals Heterogeneous nuclear ribonucleoproteins A1 and A2 modulate expression of Tid1 isoforms and EGFR signaling in non-small cell lung cancer

Oncotarget ◽  
2016 ◽  
Vol 7 (13) ◽  
pp. 16760-16772 ◽  
Author(s):  
Chi-Yuan Chen ◽  
Chia-Ing Jan ◽  
Wen-Chieh Pi ◽  
Wen-Lung Wang ◽  
Pan-Chyr Yang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Egfr Signaling ◽  
Small Cell Lung ◽  
Heterogeneous Nuclear Ribonucleoproteins

scholarly journals Trifolium Flavonoids Overcome Gefitinib Resistance of Non-Small-Cell Lung Cancer Cell by Suppressing ERK and STAT3 Signaling Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Zhiqiang Wu ◽  
Bin Xu ◽  
Zhiyi Yu ◽  
Qin He ◽  
Zhuyuan Hu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathways ◽  
Cell Line ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Stat3 Signaling ◽  
Induced Apoptosis ◽  
Gefitinib Resistance

Gefitinib is a tyrosine kinase inhibitor of EGFR (epidermal growth factor receptor) and represents the first-line treatment for EGFR mutation patients with NSCLC (non-small-cell lung cancer) therapeutics. However, NSCLC patients are inclined to develop acquired gefitinib drug resistance through nowadays, unarticulated mechanisms of chemoresistance. Here, we investigated the role of TF (Trifolium flavonoids) on sensitizing gefitinib resistance in NSCLC cells and revealed its potential mechanism of action. We demonstrated that TF exerted significantly potential chemosensitivity in gefitinib resistant NSCLC cells. MTT assay and cytological methods were used to analyze cell viability and apoptosis in NSCLC cell line PC-9R. Both TF and gefitinib suppressed PC-9R cell growth in a dose-dependent manner. Subtoxic concentrations of TF did significantly augment gefitinib-induced apoptosis in PC-9R cell line. The TF promoted chemosensitivity was major mediated by the PARP and caspases activation. Meanwhile, the TF promoted chemosensitivity also decreased the expression of Bcl-2 and Mcl-1. Finally, TF significantly reduced the phosphorylation levels of STAT3 and ERK. Altogether, the results of the present study indicated the potential mechanisms of chemosensitivity of TF in gefitinib-induced apoptosis of NSCLC by downregulating ERK and STAT3 signaling pathways and Bcl2 and Mcl-1 expression and a promising application of TF in therapy of NSCLC with gefitinib resistant.

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