1. AXL upregulates c‑Myc expression through AKT and ERK signaling pathways in breast cancers.
- Author
-
Sun, Xiaobai, Chen, Hong, You, Shuling, Tian, Zhikang, Wang, Zhaoyu, Liu, Fulin, Hu, Wenyi, Zhang, Hao, Zhang, Guoan, Zhao, Hongli, and Guo, Qingwei
- Subjects
CELLULAR signal transduction ,BREAST cancer ,WESTERN immunoblotting - Abstract
Breast cancer (BC) is common worldwide. c-Myc and AXL are both overexpressed in BC, promoting its progression. The present study aimed to investigate the role of AXL in c-Myc expression in BC. Overexpression of AXL increased c-Myc expression while knockdown of AXL decreased c-Myc expression as determined by western blot analysis. Pharmaceutical inhibition of AXL also suppressed c-Myc expression. AKT and ERK inhibitor LY294002 and U0126 suppressed c-Myc expression, respectively. AXL overexpression which activates AKT and ERK signaling, upregulates c-Myc expression, while kinase-dead AXL which cannot activate AKT and ERK signaling, does not upregulate c-Myc expression, emphasizing the important role of these two signaling pathways in c-Myc upregulation. Finally, expression data of BC tissues from The Cancer Proteome Atlas displayed an association between AXL and c-Myc. Taken together, the present study revealed that AXL upregulates c-Myc expression through AKT and ERK signaling pathways in BC. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF