scholarly journals Circ_0017639 facilitates proliferative, migratory, and invasive potential of non-small cell lung cancer (NSCLC) cells via PI3K/AKT signaling pathway

Bioengineered ◽  
2022 ◽  
Vol 13 (1) ◽  
pp. 1590-1601
Author(s):  
Hong-Bo Zhang ◽  
Xiang-Ming Qiu ◽  
Yi-Chao Zhang ◽  
Ting-Ting Huang ◽  
Zhan-Jie Zuo ◽  
...  
Tumor Biology ◽  
2011 ◽  
Vol 33 (2) ◽  
pp. 307-314 ◽  
Author(s):  
Yuanzi Yu ◽  
Dongtao Yin ◽  
Mohammad O. Hoque ◽  
Baoping Cao ◽  
Yan Jia ◽  
...  

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Baiying Li ◽  
Zuguo Yuan ◽  
Jin Jiang ◽  
Yuanquan Rao

Acquired resistance of afatinib is a significant challenge for non-small cell lung cancer (NSCLC) therapy and the mechanisms remain unclear. Aberrant activation of epidermal growth factor receptor (EGFR)-dependent downstream pathways, especially phosphatidylinositol-3-kinases/protein kinase B (PI3K/Akt) signaling pathway has been reported to be involved in the occurrence of afatinib resistance. Developing effective anti-cancer agents to overcome afatinib resistance by targetting PI3K/Akt signaling pathway will be a potential strategy for NSCLC treatment. Shikonin is a naphthoquinone compound isolated from the roots of Lithospermum erythrorhizon. In the present study, the anti-cancer activity of Shikonin was evaluated on afatinib-resistant NSCLC in vitro and in vivo. The data showed that Shikonin inhibited the proliferation and induced apoptosis of afatinib-resistant NSCLC cell line by activating apoptosis signaling pathway and negatively regulating PI3K/Akt signaling pathway. These results revealed that Shikonin was a potential apoptosis inducer in afatinib-resistant NSCLC and a promising candidate for treating patients clinically.


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