scholarly journals Inhibition of proliferation and apoptosis induced by a Na+/H+ exchanger-1 (NHE-1) antisense gene on drug-resistant human small cell lung cancer cells

2009 ◽  
Vol 21 (5) ◽  
Author(s):  
Wu
2020 ◽  
Vol 20 (2) ◽  
pp. 1256-1262
Author(s):  
Yan Huang ◽  
Ting Bao ◽  
Zhenzhen Li ◽  
Guiyi Ji ◽  
Li Zhang

Oncogene ◽  
2012 ◽  
Vol 32 (2) ◽  
pp. 209-221 ◽  
Author(s):  
M-J Jung ◽  
J-K Rho ◽  
Y-M Kim ◽  
J E Jung ◽  
Y B Jin ◽  
...  

2014 ◽  
Vol 105 (8) ◽  
pp. 1032-1039 ◽  
Author(s):  
Hiroaki Ozasa ◽  
Tetsuya Oguri ◽  
Ken Maeno ◽  
Osamu Takakuwa ◽  
Eiji Kunii ◽  
...  

2013 ◽  
Vol 335 (2) ◽  
pp. 472-478 ◽  
Author(s):  
Hiromitsu Michikoshi ◽  
Takahiro Nakamura ◽  
Katsuya Sakai ◽  
Yoshinori Suzuki ◽  
Eri Adachi ◽  
...  

2021 ◽  
Author(s):  
Mei Wang ◽  
Junyao Jiang ◽  
Yuxuan Du ◽  
Shuaimei Liu ◽  
Xiaojun Ge

Abstract Objective: Osimertinib is one of the commonly used chemotherapeutic drugs for treatment of non-small cell lung cancer (NSCLC). Nonetheless, the eventual resistance developed by cancer cells to Osimertinib has led to limitations in its application. Accordingly, there is a significant need for identifying means of reversing Osimertinib resistance.Method: The CCK-8 method was employed in detecting cell proliferation and toxicity. Western blot analysis detected protein expression, cell invasion analysis was performed using transwell assays, and the concentration of Osimertinib was determined using high performance liquid chromatography (HPLC). Result: In this study, we constructed Osimertinib-resistant cells, thus indicating the vital role of ABCG2 expression in formation of drug-resistant cells. Down-regulating ABCG2 expression in drug-resistant cells can reduce the lung cancer cells’ IC50, degree of proliferation and invasion. Combining use of ERK and PI3K inhibitors to inhibit ABCG2 expression is superior to employing a single inhibitor. Conclusion: Inhibiting the expression of ABCG2 can reverse the resistance of NSCLC cells to Osimertinib. Overexpression of ABCG2 is caused by the coactivation of the MAPK and the PI3K/AKT pathways.


Sign in / Sign up

Export Citation Format

Share Document