Sun Xiaobai, Chen Hong, You Shuling, Tian Zhikang, Wang Zhaoyu, Liu Fulin, Hu Wenyi, Zhang Hao, Zhang Guoan, Zhao Hongli, Guo Qingwei
Department of Pathology, Jinan Adicon Clinical Laboratory, Jinan, Shandong 250000, P.R. China.
Clinical Laboratory, The Third People's Hospital of Jinan, Jinan, Shandong 250132, P.R. China.
Mol Clin Oncol. 2023 Feb 8;18(3):22. doi: 10.3892/mco.2023.2618. eCollection 2023 Mar.
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.
乳腺癌（BC）在全球范围内都很常见。c-Myc和AXL在乳腺癌中均过度表达，促进其进展。本研究旨在探讨AXL在乳腺癌c-Myc表达中的作用。通过蛋白质印迹分析确定，AXL的过表达增加了c-Myc的表达，而AXL的敲低则降低了c-Myc的表达。AXL的药物抑制也抑制了c-Myc的表达。AKT和ERK抑制剂LY294002和U0126分别抑制了c-Myc的表达。激活AKT和ERK信号传导的AXL过表达上调了c-Myc的表达，而不能激活AKT和ERK信号传导的激酶失活型AXL则没有上调c-Myc的表达，这强调了这两条信号通路在c-Myc上调中的重要作用。最后，来自癌症蛋白质组图谱的乳腺癌组织表达数据显示AXL和c-Myc之间存在关联。综上所述，本研究表明AXL通过AKT和ERK信号通路在乳腺癌中上调c-Myc的表达。
