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Efficacy of abemaciclib in palbociclib-resistant hormone receptor positive breast cancer cell lines: MCF-7 and T47D

ABSTRACT: Efficacy of abemaciclib in palbociclib-resistant hormone receptor positive breast cancer cell lines: MCF-7 and T47D

PROVIDER: PRJNA920517 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23008900_1.fastq.gz	Fastqsanger.gz
	SRR23008900_2.fastq.gz	Fastqsanger.gz
	SRR23008901_1.fastq.gz	Fastqsanger.gz
	SRR23008901_2.fastq.gz	Fastqsanger.gz
	SRR23008902_1.fastq.gz	Fastqsanger.gz

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Efficacy of abemaciclib in palbociclib-resistant hormone receptor positive breast cancer cell lines: MCF-7 and T47D

Project description:Resistance to CDK4/6 inhibitors plus endocrine therapy, standard of care for HR+/HER2-neg metastatic breast cancer (MBC) patients, remains as a clinical problem with limited therapeutic options after disease progression. Treatment with abemaciclib after progression on a prior CDK4/6i has received increasing interest. However, molecular predictors of cross-resistance and unique mechanism of resistance to each CDK4/6i are unknown. In this study, multiomics analyses revealed ≥30 differentially altered pathways between palbociclib and abemaciclib resistant models. Mechanistic, preclinical and retrospective clinical evidence showed that HR+/HER2-neg MBC tumors refractory to palbociclib still may be responsive to abemaciclib. Based on the unique mechanisms of resistance to each CDK4/6i, we propose that patients who would benefit from abemaciclib treatment post progression on palbociclib could be selected based on the Hallmark gene set enrichment of G2/M pathway, while those who most probably would be refractory could be identified base on the gene set enrichment of OXPHOS pathway.

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RNA-seq transcriptome analyses in T47D cells treated with ActA and Palbociclib.

Project description:We performed SMAD2 ChIP-seq analysis in T47D cells with/without Palbociclib treatment. To validate whether the changes in SMAD2 binding to the genome indeed resulted in changes in target gene expression, we performed RNA-seq transcriptome analyses in T47D with/without ActA stimulation and Palbo treatment.

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Efficacy of abemaciclib in palbociclib-resistant hormone receptor positive organoids derived from patient derived xenografts from patients who progressed on palbociclib

Project description:Efficacy of abemaciclib in palbociclib-resistant hormone receptor positive organoids derived from patient derived xenografts from patients who progressed on palbociclib

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RNA-seq of human breast cancer cell lines MCF7 and T74D naive and resistant to palbociclib treated with capivasertib, fulvestrant and combination

Project description:T47D and MCF7 cell lines were treated with long-term (continuous) palbociclib to induce 4 resistant cell-lines (T47D RB-, T47D CDK6H, MCF7 RB- and MCF7 PacqR). Each cell line (both parental and resistant) were then treated with DMSO (control), capivasertib monotherapy, fulvestrant monotherapy and capivasertib/fulvestrant combination. RNA data is available after each treatment and resistant cell lines additionally have RNA data available after continuous palbociclib treatment.

2023-08-14 | E-MTAB-13262 | biostudies-arrayexpress

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Project description:Estrogen Receptor a (ERa) bindning to DNA was profiled by ChIP-seq in MCF-7 and T47D cells transduced with either control sgRNA, or sgRNA targeting a specific enhancer region (enhancer588). ERa in MCF-7 and T47D control or enhancer588-targeted cells

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Project description:The cellular and organismal phenotypic response to a small molecule kinase inhibitor is defined collectively by the inhibitor’s targets and their functions. The selectively of small molecule kinase inhibitors is commonly determined in vitro, using purified kinases and substrates. Recently, competitive chemical proteomics has emerged as a complementary, unbiased, cell-based approach to define the target landscape of kinase inhibitors. Here we evaluated and optimized a competitive multiplexed inhibitor bead mass spectrometry (MIB/MS) platform using cell lysates, live cells and treated mice. Several clinically active kinase inhibitors were profiled, including trametinib, BMS-777607, dasatinib, abemaciclib, and palbociclib. MIB/MS competition analyses of the cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors abemaciclib, and palbociclib revealed overlapping and unique kinase targets. Competitive MIB/MS analysis of abemaciclib revealed 83 target kinases, and dose-response profiling revealed glycogen synthase kinase 3 alpha and beta (GSK3 and GSK3 were the most potently inhibited. Cell based and in vitro kinase assays show that in contrast to palbociclib, abemaciclib directly inhibits (GSK3/β) kinase activity at low nanomolar concentrations. Consequently, abemaciclib activates β-catenin-dependent WNT signaling, as determined by β-catenin transcriptional activation and β-catenin protein stabilization. These data reveal differential kinase target specificities for CDK4/6 inhibitors may help explain differential clinical efficacy and dose-limiting toxicities. More broadly, we highlight the power of competitive chemical proteomics to identify multiple targets of kinase inhibitors in protein lysate, treated cells and in treated mice.

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Transcriptome changes in MCF-7 and T47D breast cancer cells after four day incubation in glucose deprived medium and beta-hydroxybutyrate

Project description:We investigated gene expression changes of glucose deprived MCF-7 and T47D breast cancer cells supplemented with either 10 mM or 25 mM BHB. Glucose deprivation revealed numerous differentially expressed genes indicating an involvement of the Hippo pathway in MCF-7 cells and the NRF2-Ferroptosis axis in T47D cells. Beta-hydroxybutyrate had limited impact on breast cancer cells and differentially expressed genes were not associated with any pathways following pathway enrichment analysis.

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