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Homo sapiens

ABSTRACT: H3K27Ac ChIP-seq for TL-om1 cells and primary ATL cell samples

PROVIDER: PRJNA339128 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4035090_1.fastq.gz	Fastqsanger.gz
	SRR4035090_2.fastq.gz	Fastqsanger.gz
	SRR4035100_1.fastq.gz	Fastqsanger.gz
	SRR4035100_2.fastq.gz	Fastqsanger.gz
	SRR4035091_1.fastq.gz	Fastqsanger.gz

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H3K27ac HiChIP analysis in TL-Om1 cells

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Immunomodulatory drugs (IMiDs)- or cereblon E3 ligase modulator (CELMoD)-induced growth suppression of Adult T-Cell Lymphoma/Leukemia (ATL) cells and the intrinsic rolls of cereblon for down-regulation of target proteins and their down-stream effectors II

Project description:Adult T-cell lymphoma/leukemia (ATL) is an aggressive subtype of leukemia/lymphoma caused by human T-cell leukemia virus type-1 (HTLV-1) and existing chemotherapy for ATL remains with extremely poor prognosis. Therefore, more effective therapeutic options are urgent needs for this disease. Since recent two clinical studies proved promising curability of Lenalidomide (LEN, a second-generation immunomodulatory drug [IMiDs]) for ATL patients, we investigated the direct growth-inhibitory machineries of LEN on ATL cells. Among 13 ATL-related cell lines, Hut102 and TL-Om1 exhibited best response to LEN treatment and LEN-induced functional modulation of E3-ubiquitin ligase cereblon (CRBN) induced degradation of hematopoietic-specific ikaros-family transcription factors IKZF1 and IKZF3 followed by suppression of their down-stream effectors IRF4 and c-Myc (both have been implied to promote ATL cell malignancy). Additionally, Hut102 and TL-Om1 displayed impaired expression of IKZF2 (deletion in HuT102 and altered translational variants in TL-Om1). LEN-induced growth inhibition to these two cell-lines seemed to be attributed to functional deprivation of all IKZF1/2/3. While CRBN-knockdown (KD) in HuT102 imposed LEN-resistance, IKZF2-KD in LEN-resistant ED40515 induced LEN sensitivity. DNA microarray analysis on LEN-treated HuT102 and OATL4 (LEN-resistant) displayed distinct LEN-responding transcriptional profiles; restoration of immune competency and oncogenic growth promotion respectively. Oral administration of LEN to HuT102-xenographted SCID mice demonstrated significant reduction of tumor mass. Finally, a novel form of IMiDs or cereblon modulator (CELMoD), iberdomide (IBE) exerted deeper and wider range of growth suppression to ATL cells including IKZF2 down regulation. Altogether, these findings strongly indicate the therapeutic advantages of IMiDs or CELMoD against ATL.

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Project description:We generated azacitidine (AZA)- and decitabine (DAC)-resistant (AZA-R and DAC-R, respectively) cells from drug-sensitive ATL cell lines TL-Om1 and MT-2 via long-term drug exposure. To identify molecular mechanisms responsible for acquired resistance, we performed transcriptome analysis using Clariom S microarray.

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Homo sapiens

Project description:RNA Pol II ChIP-seq analysis after THZ1 treatment in TL-Om1 cells

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H3K27ac HiChIP analysis in TL-Om1 cells

Project description:H3K27ac HiChIP analysis in TL-Om1 cells

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