Metabolomic Profiling Reveals Key Metabolic Alterations in MCF7 Tamoxifen-Resistant Cells Following EPAS1 Inhibition

Tamoxifen (TAM) is a frontline therapy for luminal A breast cancer, yet acquired resistance poses a significant clinical challenge. This study investigates the molecular and metabolic basis of TAM resistance in MCF7/Tam1 cells, focusing on EPAS1 (HIF-2α)-driven hypoxia-induced metabolic reprogrammin...

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Detaylı Bibliyografya
Yazar:	Enzhi Luo (21737638) (author)
Diğer Yazarlar:	Neeraj Manvi Agarwal (21737641) (author), Junjeong Choi (795304) (author)
Baskı/Yayın Bilgisi:	2025
Konular:	Biochemistry Microbiology Cell Biology Genetics Physiology Pharmacology Biotechnology Cancer Hematology Computational Biology Chemical Sciences not elsewhere classified significant clinical challenge promising therapeutic strategy fatty acid oxidation mediated metabolic reprogramming induced metabolic reprogramming support epas1 inhibition findings highlight epas1 enhanced glutamine metabolism restore tam sensitivity epas1 inhibitor pt2977 metabolic pathways metabolic basis epas1 along lipid metabolism glutathione metabolism warburg effect venn analyses untargeted lc tam1 cells tam stress tam resistance study investigates selective reduction resistant cells redox balance pt2977 disrupted overcome resistance notable dysregulation metabolite profiles key driver including jak frontline therapy dependent normalization cell viability cell survival breast cancer associated pathways
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Metabolomic Profiling Reveals Key Metabolic Alterations in MCF7 Tamoxifen-Resistant Cells Following EPAS1 Inhibition

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