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ANXA1 promotes cell proliferation and drug-resistance in B cell acute lymphoblastic leukemia

ABSTRACT: ANXA1 promotes cell proliferation and drug-resistance in B cell acute lymphoblastic leukemia

PROVIDER: PRJNA940356 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23689290.fastq.gz	Fastqsanger.gz
	SRR23689291.fastq.gz	Fastqsanger.gz
	SRR23689292.fastq.gz	Fastqsanger.gz
	SRR23689293.fastq.gz	Fastqsanger.gz
	SRR23689294.fastq.gz	Fastqsanger.gz

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ANXA1 promotes cell proliferation and drug-resistance in B cell acute lymphoblastic leukemia

Project description:ANXA1 promoted cell proliferation, suppressed cell apoptosis induced cell cycle arrest in B-ALL cells by CCK8, Flow cytometry and RNA-seq Sequencing analysis. The in vivo results indicated that down-regulation of ANXA1 in B-ALL cells could significantly reduce leukemic cell burden. We then performed gene expression profiling using data obtained from RNA-seq of B-ALL cells with the ANXA1 gene down-regulated in CCRF-SB.

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miRNA expression data from MCF-7 cells, overexpressing ANXA1

Project description:Annexin 1 (ANXA1), an endogenous anti-inflammatory protein which modulates cellular processes such as proliferation, differentiation and apoptosis has been implicated in cancer initiation and progression. ANXA1 was previously shown to be regulated by hsa-miR-196a and promoted cell proliferation and anchorarge-dependent growth and suppressed apoptosis. However, whether ANXA1 itself regulates miRNA expression is unknown. Therefore, in this study, we investigated the regulation of miRNA by ANXA1 in breast cancer cells. Using microarray technology, 12 miRNAs were found to be significantly and consistently downregulated in MCF-7 cells (MCF-V5) overexpressing ANXA1 overexpressing MCF-7 cells (MCF-V5). Hsa-miR-26b* and hsa-miR-562 were chosen for further investigation.The data suggest that miR-26b* and miR-562 may play a role in ANXA1-induced migration and possibly angiogenesis by targeting NFKB and point towards a potential therapeutic target for breast cancer. Breast cancer MCF-7 cells (MCF-V5) overexpressing ANXA1 were cultured for RNA extraction and hybridization on Affymetrix miRNA microarrays. These were compared against the control, which were MCF-7 cells (MCF-EV) carrying an empty expression vector. Expression analyses were carried out in triplicates

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miRNA expression data from MCF-7 cells, overexpressing ANXA1

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Proteomics analysis of childhood acute lymphoblastic leukemia cell lines reveals novel drug vulnerabilities

Project description:Acute lymphoblastic leukemia (ALL) is the most common childhood cancer, and it has a 5-year survival rate of 85% for European children. But for subsets of patients who fail to respond to standard of care chemotherapeutics, treatment options are limited, and clinical prognosis is poor. To establish a platform and methodology to better characterize ALL subtypes and identify their pharmacologic vulnerabilities, we assembled a biobank of 49 readily available childhood ALL cell lines representing diverse immunotypes and genetic profiles. Using these cell lines, we performed comprehensive multi-omic analyses, providing proteomic, transcriptomic and pharmacoproteomic characterization of childhood ALL. We used this resource to characterize the functional impact of genetic fusions and cellular differentiation states on the proteome. Additionally, we identified a novel drug vulnerability in one of the ALL subtypes. Our results are provided as an interactive online data portal with navigable proteomics, transcriptomics, and drug sensitivity profiles.

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Project description:To investigate the effect of ANXA1, encoding annexin a1, on group 2 innate lymphoid cells (ILC2s), we downregulated the expression using lentiviral vector-based shRNA transfer and performed RNA-seq analysis.

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Absence of Anxa1 in myeloid lineage cells exacerbates acute pancreatitis (AP)

Project description:To elucidate the role of macrophage Anxa1 in the pathogenesis of AP, we intercrossed Anxa1flox/flox (Anxa1f/f or Anxa1 WT, as control) with Lyz2-Cre mice to create myeloid-specific Anxa1-knockout (Anxa1CKO) mice. We induced AP with repeated injection of cerulein in Anxa1CKO and Anxa1f/f littermates and examined the pancreas injury and inflammation. Pancreas tissue samples were collected at 12 hours after the first cerulein injection and performed RNA-seq.

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