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ERO1A promotes lung cancer progression via HIF1A/EGFR
Yue Liu1, Yiyan Lin2, Yi Zhou1
1Department of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, SUSTech Homeostatic Medicine Institute, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Abstract:
Globally, lung cancer has emerged as a formidable public health challenge and is the primary cause of cancer-related deaths. The role of ERO1A in lung adenocarcinoma has been rarely explored. Here, we identified significant overexpression of ERO1A in lung cancer tissues, which correlates with reduced patient survival rates. Silencing ERO1A notably suppressed cell proliferation, clonogenic formation, migration, and invasion in lung cancer cell lines. ERO1A inhibition impairs tumor growth in murine models. RNA sequencing and proteomics analyses following ERO1A knockdown revealed that ERO1A is involved in multiple oncogenic pathways, particularly EGFR and HIF1A. ERO1A modulates HIF1A/EGFR may through H₂O₂. The oncogenes MET, CCND1, and p21 may also be involved in the ERO1A regulation pathway. The upregulation of ERO1A may serve as a valuable diagnostic and prognostic biomarker in lung cancer. The ERO1A-HIF1A/EGFR axis may represent a potential therapeutic target.
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