Association of tamoxifen resistance and lipid reprogramming in breast cancer

BMC Cancer
Susanne HultschOlli Kallioniemi

Abstract

Tamoxifen treatment of estrogen receptor (ER)-positive breast cancer reduces mortality by 31%. However, over half of advanced ER-positive breast cancers are intrinsically resistant to tamoxifen and about 40% will acquire the resistance during the treatment. In order to explore mechanisms underlying endocrine therapy resistance in breast cancer and to identify new therapeutic opportunities, we created tamoxifen-resistant breast cancer cell lines that represent the luminal A or the luminal B. Gene expression patterns revealed by RNA-sequencing in seven tamoxifen-resistant variants were compared with their isogenic parental cells. We further examined those transcriptomic alterations in a publicly available patient cohort. We show that tamoxifen resistance cannot simply be explained by altered expression of individual genes, common mechanism across all resistant variants, or the appearance of new fusion genes. Instead, the resistant cell lines shared altered gene expression patterns associated with cell cycle, protein modification and metabolism, especially with the cholesterol pathway. In the tamoxifen-resistant T-47D cell variants we observed a striking increase of neutral lipids in lipid droplets as well as an accumulation of fr...Continue Reading

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Datasets Mentioned

BETA
GSE111151

Methods Mentioned

BETA
exome sequencing
FCS
chip
Assay
PCA

Software Mentioned

subreadR
EnsEMBL
biomaRt
Enricher
limma
edgeR
Enrichr
ImageJ
FusionCatcher

Related Concepts