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AXL upregulates c‑Myc expression through AKT and ERK signaling pathways in breast cancers

AXL upregulates c‑Myc expression through AKT and ERK signaling pathways in breast cancers 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular and Clinical Oncology Spandidos Publications

AXL upregulates c‑Myc expression through AKT and ERK signaling pathways in breast cancers

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Publisher
Spandidos Publications
Copyright
Copyright \xC2\xA9 2023 Spandidos Publications
ISSN
2049-9450

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.

Journal

Molecular and Clinical Oncology – Spandidos Publications

Published: Mar 17, 2023

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