Apatinib enhances antitumour activity of EGFR-TKIs in non-small cell lung cancer with EGFR-TKI resistance

2017 ◽  
Vol 84 ◽  
pp. 184-192 ◽  
Author(s):  
Fang Li ◽  
Tengjiao Zhu ◽  
Baoshan Cao ◽  
Jiadong Wang ◽  
Li Liang
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Antitumour Activity ◽  
Small Cell ◽  
Small Cell Lung ◽  
Tki Resistance ◽  
Egfr Tki ◽  
Egfr Tkis

scholarly journals Downregulation of miR-506-3p Facilitates EGFR-TKI Resistance through Induction of Sonic Hedgehog Signaling in Non-Small-Cell Lung Cancer Cell Lines

2020 ◽  
Vol 21 (23) ◽  
pp. 9307
Author(s):  
Inamul Haque ◽  
Hameem I. Kawsar ◽  
Hannah Motes ◽  
Mukut Sharma ◽  
Snigdha Banerjee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Sonic Hedgehog ◽  
Cell Lung Cancer ◽  
Molecular Mechanisms ◽  
Small Cell ◽  
Small Cell Lung ◽  
Mesenchymal Transition ◽  
Tki Resistance ◽  
Egfr Tki

Non-small-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutation eventually develop resistance to EGFR-targeted tyrosine kinase inhibitors (TKIs). Treatment resistance remains the primary obstacle to the successful treatment of NSCLC. Although drug resistance mechanisms have been studied extensively in NSCLC, the regulation of these mechanisms has not been completely understood. Recently, increasing numbers of microRNAs (miRNAs) are implicated in EGFR-TKI resistance, indicating that miRNAs may serve as novel targets and may hold promise as predictive biomarkers for anti-EGFR therapy. MicroRNA-506 (miR-506) has been identified as a tumor suppressor in many cancers, including lung cancer; however, the role of miR-506 in lung cancer chemoresistance has not yet been addressed. Here we report that miR-506-3p expression was markedly reduced in erlotinib-resistant (ER) cells. We identified Sonic Hedgehog (SHH) as a novel target of miR-506-3p, aberrantly activated in ER cells. The ectopic overexpression of miR-506-3p in ER cells downregulates SHH signaling, increases E-cadherin expression, and inhibits the expression of vimentin, thus counteracting the epithelial–mesenchymal transition (EMT)-mediated chemoresistance. Our results advanced our understanding of the molecular mechanisms underlying EGFR-TKI resistance and indicated that the miR-506/SHH axis might represent a novel therapeutic target for future EGFR mutated lung cancer treatment.

scholarly journals Apatinib combined with EGFR-TKI in treating advanced non-small cell lung cancer with EGFR-TKI resistance

2019 ◽  
Vol 30 ◽  
pp. v625-v626
Author(s):  
R. Tian ◽  
W. Guo ◽  
Y. Guo ◽  
X. Zhang ◽  
H. Zhu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Tki Resistance ◽  
Egfr Tki

scholarly journals Targeting the miR-200c/LIN28B axis in acquired EGFR-TKI resistance non-small cell lung cancer cells harboring EMT features

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Hiroki Sato ◽  
Kazuhiko Shien ◽  
Shuta Tomida ◽  
Kazuhiro Okayasu ◽  
Ken Suzawa ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Tki Resistance ◽  
Egfr Tki

scholarly journals Lymecycline reverses acquired EGFR-TKI resistance in non–small-cell lung cancer by targeting GRB2

2020 ◽  
Vol 159 ◽  
pp. 105007 ◽  
Author(s):  
Yang Chen ◽  
Jie Wu ◽  
Hongfei Yan ◽  
Yang Cheng ◽  
Yizhe Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Tki Resistance ◽  
Egfr Tki
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