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Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

ABSTRACT: Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

PROVIDER: PRJNA1022781 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26241959_1.fastq.gz	Fastqsanger.gz
	SRR26241959_2.fastq.gz	Fastqsanger.gz
	SRR26241960_1.fastq.gz	Fastqsanger.gz
	SRR26241960_2.fastq.gz	Fastqsanger.gz
	SRR26241961_1.fastq.gz	Fastqsanger.gz

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Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

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Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

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Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

Project description:We assessed the chromatin localization of XPO1 and p300 in response to C646 (10 uM), S109 (1 uM), and SP100030 (1 uM). We used CUT&RUN sequencing as a lower-input (500,000 cells per sample), higher-sensitivity alternative to ChIP-Seq to assess chromatin binding of different factors

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Prolonged XPO1 inhibition is essential to achieve optimal antileukemic activity in NPM1-mutated acute myeloid leukemia

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Discovery, Validation and Mechanistic study of XPO1 inhibition in the Treatment of Triple Negative Breast Cancer

Project description:Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer with limited treatment options. This study investigates the potential of repurposing selinexor, an XPO1 inhibitor, as a novel therapeutic option for TNBC. By utilizing a computational drug repurposing approach, XPO1 inhibitors were identified to be preferentially sensitive in TNBC compared to other breast cancer subtypes and its efficacy validated in an independent patient dataset and across various TNBC cell lines. Using RNA-sequencing after longitudinal XPO1 inhibition in a panel of TNBC cell lines and western blotting, we reveal that XPO1 inhibitor induces TNBC cell death by inhibiting the NF-kB pathway through nuclear retention of NFKBIA, a key regulator of this pathway. These findings suggest that XPO1 inhibitors could be an effective targeted therapy for TNBC and paves the way for more personalized treatment strategies offering hope for better outcomes in TNBC patients.

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XPO1 amplification abrogates the effects of E571K XPO1 mutation in B-cell lymphoma

Project description:XPO1 gene encodes exportin 1 (XPO1) that controls the nuclear export of cargo proteins and RNAs. Almost 25% of primary mediastinal B-cell lymphomas (PMBL) and classical Hodgkin lymphomas (cHL) cases harboured a recurrent XPO1 point mutation (NM_003400, chr2:g61718472C>T) resulting in the E571K modification within the hydrophobic groove of the protein, the site of cargo proteins binding. We investigated the functional impact of XPO1E571K mutation using cell lines having various XPO1 status. We first confirmed that the mutation was present both within the XPO1 mRNA and the corresponding protein. In the U2940 cell line having a wild-type (wt) XPO1 gene, we introduced the E571K mutation using several CRISPR-Cas9 strategies. Using a barcoding method to trace the mutation, we observed that the mutation gave no advantage in vitro. Indeed, the effects of XPO1E571K mutation were hidden by the presence of the XPO1 wt allele. Strikingly, XPO1E571K mutation never occurred as homozygous or hemizygous in our patients�� cohort. We further showed that XPO1E571K mutation modified selinexor binding to XPO1 and in turn, its sensitivity to this drug. We concluded that the balance between the wild-type and the mutated allele of XPO1 is a key element in defining XPO1 functions and oncogenic properties.

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2025-03-28 | GSE270396 | GEO

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