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作者

Xiaobai Sun Hong Chen Shuling You Zhikang Tian Zhaoyu Wang Fulin Liu Wenyi Hu Hao Zhang Guoan Zhang Hongli Zhao Qingwei Guo

作者单位

Affiliations ¹ Department of Pathology, Jinan Adicon Clinical Laboratory, Jinan, Shandong 250000, P.R. China. ² Clinical Laboratory, The Third People's Hospital of Jinan, Jinan, Shandong 250132, P.R. China. ³ College of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China. ⁴ Institute of Forensic Medicine and Laboratory Medicine, Jining Medical University, Forensic Science Center of Jining Medical University, Jining, Shandong 272067, P.R. China. ⁵ Department of Digestive System, Shandong Institute of Parasitic Diseases, Shandong First Medical University and Shandong Academy of Medical Sciences, Jining, Shandong 272067, P.R. China. ⁶ Department of Hematology, Jinan Children's Hospital, Jinan, Shandong 250132, P.R. China.

刊名

Molecular and clinical oncology

年份

2023

卷号

Vol.18 No.3

页码

22

ISSN

2049-9469

关键词

AXL breast cancer c-Myc.

摘要

Breast cancer 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 wh...更多

Breast cancer 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.收起

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