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Adaptive responses of the HER2+ SKBR-3 and BT474m1 cell lines to lapatinib and JQ1

ABSTRACT: Adaptive responses of the HER2+ SKBR-3 and BT474m1 cell lines to lapatinib and JQ1

PROVIDER: PRJNA671649 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12888286.fastq.gz	Fastqsanger.gz
	SRR12888287.fastq.gz	Fastqsanger.gz
	SRR12888288.fastq.gz	Fastqsanger.gz
	SRR12888289.fastq.gz	Fastqsanger.gz
	SRR12888290.fastq.gz	Fastqsanger.gz

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Adaptive responses of the HER2+ SKBR-3 and BT474m1 cell lines to lapatinib and JQ1

Project description:SKBR-3 or BT474m1 HER2+ breast cancer cells were treated with either DMSO, 300nM lapatinib, 300nM JQ1, or lapatinib and JQ1 in combination for 48h.

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Enhancer analysis of HER2+ cell lines SKBR-3 (ER-) and BT474m1 (ER+) in response to lapatinib and JQ1 and analysis of FOXA1 chromatin binding in SKBR-3 cells in response to lapatinib and JQ1 and impact of FOXA1 knockdown on BRD4 and MED1

Project description:SKBR-3 and BT474m1 HER2+ breast cancer cell lines were treated with lapatinib, JQ1, or lapatinib and JQ1 or (for SKBR-3) treated with siRNA pools (non-targeting control or FOXA1) prior to drug treatment before being used for ChIPseq (BRD4, MED1, H3K27Ac, or FOXA1 (for SKBR-3))

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FOXA1-dependent responses of the HER2+ SKBR-3 cell line to lapatinib

Project description:FOXA1-dependent responses of the HER2+ SKBR-3 cell line to lapatinib

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Project description:Enhancer analysis of HER2+ cell lines SKBR-3 (ER-) and BT474m1 (ER+) in response to lapatinib and JQ1 and analysis of FOXA1 chromatin binding in SKBR-3 cells in response to lapatinib and JQ1 and impact of FOXA1 knockdown on BRD4 and MED1

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Project description:Inhibition of the HER2/ERBB2 receptor is a keystone to treating HER2-positive malignancies, particularly breast cancer, but a significant fraction of HER2-positive (HER2+) breast cancers recur or fail to respond. Anti-HER2 monoclonal antibodies, like trastuzumab or pertuzumab, and ATP active site inhibitors like lapatinib, commonly lack durability because of adaptive changes in the tumor leading to resistance. HER2+ cell line responses to inhibition with lapatinib were analyzed by RNAseq and ChIPseq to characterize transcriptional and epigenetic changes. Motif analysis of lapatinib-responsive genomic regions implicated the pioneer transcription factor FOXA1 as a mediator of adaptive responses. Lapatinib in combination with FOXA1 depletion led to dysregulation of enhancers, impaired adaptive upregulation of HER3, and decreased proliferation. HER2-directed therapy using clinically relevant drugs (trastuzumab with or without lapatinib or pertuzumab) in a 7-day clinical trial designed to examine early pharmacodynamic response to antibody-based anti-HER2 therapy showed reduced FOXA1 expression was coincident with decreased HER2 and HER3 levels, decreased proliferation gene signatures, and increased immune gene signatures. This highlights the importance of the immune response to anti-HER2 antibodies and suggests that inhibiting FOXA1-mediated adaptive responses in combination with HER2 targeting is a potential therapeutic strategy.

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