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Chidamide effect on MM

ABSTRACT: Chidamide effect on MM

PROVIDER: PRJNA658123 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12478010_1.fastq.gz	Fastqsanger.gz
	SRR12478010_2.fastq.gz	Fastqsanger.gz
	SRR12478011_1.fastq.gz	Fastqsanger.gz
	SRR12478011_2.fastq.gz	Fastqsanger.gz
	SRR12478012_1.fastq.gz	Fastqsanger.gz

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Chidamide used in MM primary cells [RNA-seq]

Project description:Most patients with multiple myeloma (MM) will eventually relapse and current treatments have limited effect. Herein, we demonstrate that succinate dehydrogenase subunitA (SDHA) was low expressed in MM patients, and patients with SDHA relatively high expression had long overall survival and progression-free survival. Furthermore, SDHA high expression inhibited proliferation and invasion in multiple myeloma (MM) cell lines and enhanced the anti-tumor and synergistic effect of chemotherapeutics. We conducted transcriptome comparison of BMMCs of three MM patients treated with DMSO or chidamide.

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Chidamide used in MM cell line [ChIP-seq]

Project description:Most patients with multiple myeloma (MM) will eventually relapse and current treatments have limited effect. Herein, we demonstrate that succinate dehydrogenase subunitA (SDHA) was low expressed in MM patients, and patients with SDHA relatively high expression had long overall survival and progression-free survival. Furthermore, SDHA high expression inhibited proliferation and invasion in multiple myeloma (MM) cell lines and enhanced the anti-tumor and synergistic effect of chemotherapeutics. To investgate regulation of SDHA on epigenetic level, we conducted ChIP-seq experiments to compare the H3K27ac signal between H929 cells treated with DMSO and H929 cells treated with chidamide.

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Chidamide used in MM primary cells [RNA-seq]

Project description:Chidamide used in MM primary cells [RNA-seq]

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Chidamide used in MM cell line [ChIP-seq]

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Chidamide inhibits the NOTCH1-MYC signaling axis in T-cell acute lymphoblastic leukemia

Project description:We report that Chidamide shows significant anti- proliferation and more specifically anti-NOTCH effects in both cell lines and primary cells of T-ALL patients. By analyzing the expression profile characterizing the response of the cell lines to Chidamide treatment, we further confirmed that the antitumor effect of Chidamide was due to the inhibition of HDAC and the anti-NOTCH1 effect.

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Chidamide effect on MM

Project description:This SuperSeries is composed of the SubSeries listed below.

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Aberrant JAK-STAT pathway confers resistance to the HDAC inhibitor chidamide in Natural Killer/T-cell lymphoma through chromatin remodeling

Project description:Natural Killer/T-cell lymphoma (NKTL) is a rare type of aggressive and heterogeneous non-Hodgkin's lymphoma (NHL) with poor prognosis and limited therapeutic options. Here, we demonstrate that chidamide, a novel histone deacetylase (HDAC) inhibitor, is effective in treating relapsed/refractory NKTL patients, achieving an overall response rate of 39.3%, with 17.9% complete response rate. However, the clinical response to chidamide remains variable as more than half of the patients exhibit primary resistance, limiting its utility in NKTL treatment. To unravel the resistance mechanisms of chidamide, we performed integrative transcriptomic and chromatin profiling of sensitive and resistant NKTL cells. Our results revealed that aberrant JAK-STAT signaling remodels the chromatin and confers resistance to chidamide. Subsequently, inhibition of JAK-STAT activity could overcome resistance to chidamide by reprogramming the chromatin from a resistant to sensitive state, leading to synergistic anti-tumor effect. More importantly, our clinical data demonstrated that combinatorial therapy with chidamide and JAK inhibitor ruxolitinib is effective against chidamide-resistant NKTL. In addition, we identified TNFRSF8 (CD30), a downstream target of JAK-STAT pathway, as a potential biomarker that could predict NKTL sensitivity to chidamide. Collectively, our study suggests that chidamide, in combination with JAK-STAT inhibitors, can be a novel targeted therapy in the standard of care for NKTL.

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