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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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BCL2 targeting overcomes the microenvironment-induced resistance to crizotinib in ALK+ anaplastic large cell lymphoma

ABSTRACT: Drug sensitivity assessment of two different ALCL cell lines growth with or without mouse cell line co-culture

INSTRUMENT(S): NextSeq 550

ORGANISM(S): Homo sapiens

SUBMITTER: Pietro Zoppoli

PROVIDER: E-MTAB-14526 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Functional effect of DOT1L pharmacological inhibition in ERα-positive Ovarian Cancer cells

Project description:Estrogen Receptor alpha (ERα), a nuclear receptor with transcriptional activity, is a master regulator of estrogen signaling, widely known as therapeutic target in hormone-responsive breast cancer (BC). Moreover, ERα is highly expressed in approximately 80% of High Grade Serous Ovarian Cancer (HGSOC), the most common epithelial ovarian carcinoma. Despite some promising clinical trials evaluating endocrine therapy in this type of tumor, the role of ERα is still unknown. Epigenetic changes, such as DNA methylation, are emerging as key contributing factors to carcinogenesis. Disruptor of telomeric silencing-1-like (DOT1L), the only known histone methyl transferase capable to produce H3K79 mono, di and tri-methylation, modulates ERα actions in hormone-responsive BC. Considering this evidence, ERα-DOT1L association was confirmed in ERα-positive OC cells, PEO1 and PEO4, by Co-IP. DOT1L pharmacological inhibition by EPZ004777 (EPZ) revealed the involvement of this epigenetic enzyme in cell proliferation, cell cycle progression and apoptosis. Transcriptome profiling after ICI (a Selective Estrogen Receptor Degrader) and EPZ treatment, in both cell lines, has underlined a deep impact of both compounds on ERα-modulated genes, including the down-regulation of ERα itself. On the other hand, functional analysis showed that commonly affected transcripts are involved in different cellular processes, such as cancer cell survival, chemoresistance and cell cycle progression. Moreover, ChIP-qPCR performed on ERα promoter highlighted ERα and DOT1L co-localization, both in PEO1 and in PEO4 cells, which was reduced after EPZ treatment, suggesting a role of this complex on receptor transcriptional activity. In addition, drug combination studies performed with EPZ and ICI showed an additive effect in cell growth inhibition. Taken together, these results suggest DOT1L as a potential therapeutic target in the treatment of OC.

2019-11-04 | E-MTAB-8198 | biostudies-arrayexpress

Inhibition of the histone methyltrasferares DOT1L deregulates hormone responsive breast cancer cells methylome

Project description:Estrogen Receptor αlpha (ERα) is the master regulator of estrogen signaling in hormone-responsive breast cancer (BC), however epigenetic mechanisms, including DNA methylation, are emerging as key processes for regulation of critical cell functions including tumorigenesis. We have recently reported the epigenetic writer DOT1L (DOT1 Like Histone Lysine Methyltransferase) to associated to ERα, part of chromatin bound multiprotein complex and that the pharmacological inhibition of this enzyme reduces the transcription rate of several genes involved in ERα-mediated signaling leading to inhibition of BC cell proliferation. Here, we investigated the functional impact of DOT1L inhibition on methylome changes in BC and its possible contribution to deregulation of transcriptional pathways associated to the progression of this disease.

2023-02-21 | E-MTAB-12635 | biostudies-arrayexpress

Cabozantinib overcomes crizotinib resistance in ROS1 fusion-positive cancer.

Project description: Not available

| S-EPMC4286456 | biostudies-literature

Dasatinib overcomes AML cells resistant to BCL2 inhibition by degrading MCL1.

Project description: Not available

| S-EPMC12378904 | biostudies-literature

Venetoclax Overcomes Sorafenib Resistance in Acute Myeloid Leukemia by Targeting BCL2.

Project description: Not available

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Low pass whole methylome enzymatic sequencing of four AML cell lines untreated and after treatment with different concentrations of 5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC), Cytarabine (ARAC) and GSK3685032 (GSK5032) for 3 and 7 days

Project description:We conducted low-coverage whole-genome enzymatic methylation sequencing (EM-seq) on four commercially available AML cell lines to assess their global DNA methylation profiles following treatment with varying concentrations (0–3000 nM) of three different hypomethylating agents—5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC), and GSK3685032 (GSK5032)—for 3 and 7 days (only GSK5032), as well as Cytarabine (ARAC) for 3 days.

2025-04-10 | E-MTAB-14969 | biostudies-arrayexpress

RNA-Seq of An Integrated Signaling Network Controls P-Bodies Dynamics and mRNA Translation in Human Glioblastoma

Project description:Processing (P)-bodies are cytoplasmic membrane-less condensates including translationally repressed mRNAs and proteins involved in the mRNA decay machinery. The mechanisms underlying P-bodies nucleation and mRNA decay have been largely described. However, the impact of signaling networks in P-bodies dynamics and mRNA translation is still not well understood. Here, we identify a ribonucleoprotein network assembled by the E3 ubiquitin ligase Praja2 at P-bodies that coordinates protein translation and mRNA turnover in human glioblastoma (GBM). Praja2 physically interacts and spaBally co-localizes with the RNA helicase DDX6, a core component and nucleating factor of P-bodies. Stimulation of the G protein-coupled receptor (GPCR)-cAMP pathway in GBM cells induces a non-proteolytic polyubiquitylation of DDX6 by Praja2. DDX6 ubiquitylation is required for P-bodies assembly and mRNA translation repression. Interfering with DDX6 ubiquitylation or downregulation of expression markedly affects P-bodies assembly. Moreover, geneBc deleBon of praja2 dramatically impacts the assembly of DDX6/mRNA complexes and the amount of translating polysomes, leading to cellular senescence and GBM growth arrest. These findings identify a cAMP-driven post-transcriptional control mechanism operating at P- bodies by the ubiquitin system that profoundly impacts on mRNA translation and cancer cell growth. This regulatory system may, thus, contribute to the adaptive metabolic rewiring underlying cancer growth and drug resistance.

2025-03-30 | E-MTAB-14326 | biostudies-arrayexpress

The ALK inhibitor ceritinib overcomes crizotinib resistance in non-small cell lung cancer.

Project description: Not available

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Small RNA-seq analysis of serum miRNAs from patients with systemic sclerosis, Raynaud’s phenomenon, and healthy controls

Project description:Systemic sclerosis (SSc) is a complex autoimmune disease characterized by microvascular dysfunction, immune dysregulation, and progressive fibrosis, and can be classified into limited cutaneous (lcSSc) and diffuse cutaneous (dcSSc) forms. Primary Raynaud’s phenomenon (RP) is a functional vascular disorder that may precede or occur independently of connective tissue diseases. Circulating microRNAs (miRNAs) have emerged as regulators of vascular and immune processes and can be detected in serum. In this study, serum miRNA profiles were assessed in patients with SSc, including lcSSc and dcSSc subtypes, RP, and healthy controls. Small RNA sequencing was performed in a discovery cohort to characterize circulating miRNA expression across the study groups. Libraries were prepared from serum-derived RNA and sequenced on an Illumina platform. Raw sequencing data were processed using a standardized pipeline for miRNA quantification, and normalized counts were generated for downstream analyses. This dataset provides a resource for the exploration of circulating miRNA profiles in SSc subtypes and RP.

2026-04-01 | E-MTAB-16866 | biostudies-arrayexpress

RNA-seq data of wildtype and ZNF334-edited THP-1 cell lines with or without cold stimulation

Project description:RNA-seq was performed to identify differences in the transcriptome between wildtype, ZNF334 +/- and ZNF334 -/- THP-1 cells with or without cold stimulation.

2025-12-01 | E-MTAB-15463 | biostudies-arrayexpress

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