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Gene expression profile at single cell level of bone marrow cells in 5TGM1 multiple myeloma mouse model of NEK2 deficiency

ABSTRACT: Gene expression profile at single cell level of bone marrow cells in 5TGM1 multiple myeloma mouse model of NEK2 deficiency

PROVIDER: PRJNA941249 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23706835.fastq.gz	Fastqsanger.gz
	SRR23706836.fastq.gz	Fastqsanger.gz
	SRR23706837.fastq.gz	Fastqsanger.gz
	SRR23706838.fastq.gz	Fastqsanger.gz
	SRR23706839.fastq.gz	Fastqsanger.gz

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Gene expression profile at single cell level of bone marrow cells in 5TGM1 multiple myeloma mouse model of NEK2 deficiency

Project description:To determine how the lack of NEK2 in the tumor microenvironmental cells contributes to tumor inhibition and immune regulation, we used single cell RNA sequencing (scRNA-seq) to analyze the diversity of immune cells in the bone marrow of 5TGM1 MM mouse model with and without NEK2 deficiency.

2023-06-01 | GSE226697 | GEO

Transcription profiling of human bone marrow from primary multiple myeloma patients

Project description:Drug resistance is a major obstacle in cancer therapy. The molecular mechanisms of drug resistance still remain largely elusive. Microarray analyses on paired primary myeloma samples at baseline and after therapy or at relapse showed that NEK2 was one of the most up-regulated genes in myeloma cells after high-dose chemotherapy or at relapse. By analyzing the published (> 2,500) microarrays and clinical datasets, we found that NEK2 expression is increased in many malignancies, and that high expression of NEK2 was associated with a shorter event-free and overall survival. Moreover, NEK2 expression was typically increased in tumors with aggressive subtype and advanced TNM stage. Our studies indicate that over-expressing NEK2 in cancer cells resulted in enhanced cell proliferation and drug resistance, whereas knockdown of NEK2 induced significant cancer cell death and growth inhibition. We found that NEK2 over-expression activates cell cycle progression and cell division through the stimulation of cell cycling genes CDC2/CCNB1 and PBK. Interestingly, NEK2-overexpression also activated the Wnt/Î²-catenin signaling pathway. We conclude that NEK2 represents a predictor for drug resistance and poor prognosis in cancers and could be a potential target for cancer therapy. Experiment Overall Design: Myeloma tumor cells from bone marrow aspirates were collected at baseline and after chemotherapy (pre-1st and pre-2nd bone marrow transplant, and pre-consolidation) for RNA extraction and hybridization on Affymetrix microarrays. We sought to define genes related to chemotheraputic resistance.

2010-01-30 | E-GEOD-19554 | biostudies-arrayexpress

Expression data from bone marrow of primary multiple myeloma patients

Project description:Drug resistance is a major obstacle in cancer therapy. The molecular mechanisms of drug resistance still remain largely elusive. Microarray analyses on paired primary myeloma samples at baseline and after therapy or at relapse showed that NEK2 was one of the most up-regulated genes in myeloma cells after high-dose chemotherapy or at relapse. By analyzing the published (> 2,500) microarrays and clinical datasets, we found that NEK2 expression is increased in many malignancies, and that high expression of NEK2 was associated with a shorter event-free and overall survival. Moreover, NEK2 expression was typically increased in tumors with aggressive subtype and advanced TNM stage. Our studies indicate that over-expressing NEK2 in cancer cells resulted in enhanced cell proliferation and drug resistance, whereas knockdown of NEK2 induced significant cancer cell death and growth inhibition. We found that NEK2 over-expression activates cell cycle progression and cell division through the stimulation of cell cycling genes CDC2/CCNB1 and PBK. Interestingly, NEK2-overexpression also activated the Wnt/β-catenin signaling pathway. We conclude that NEK2 represents a predictor for drug resistance and poor prognosis in cancers and could be a potential target for cancer therapy.

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Effect of NEK2 deficiency on gene expression of CD19-selected spleen B cells of Eμ-myc mouse model

Project description:NEK2 overexpression in the B cell lineage affects B cell development. To determine whether deficiency of NEK2 inhibits B cell malignancies, we crossed Nek2 knockout mice with Eμ-myc transgenic mice, a well-established Myc-driven preclinical model for B cell malignancies. Three genotyping offsprings were obtained: Eμ-myc/Nek2+/+ (NEK2 wild type), Eμ-myc/Nek2+/- (NEK2 heterozygotes), and Eμ-myc/Nek2-/- (NEK2 homozygotes). Bulk RNA-seq was performed on CD19-selected spleen B cells to view the transcriptome differences.

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Targeting NEK2 impairs oncogenesis and radioresistance via inhibiting the Wnt1/β-catenin signaling pathway in cervical cancer

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Gene expression profile at single cells level of liver tissues in Nek2 conditioned-knock out mice model (Nek2f/f lyz2cre)

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2024-08-31 | GSE275911 | GEO

Multiple myeloma-derived extracellular vesicles modulate the bone marrow immune microenvironment

Project description:One of the hallmarks of multiple myeloma (MM) is a permissive BM microenvironment. Increasing evidence suggest that cell-to-cell communication between myeloma and immune cells via tumor cell-derived extracellular vesicles (EV) plays a key role in the pathogenesis of MM. Hence, we aimed to explore BM immune alterations induced by MM-derived EV. For this, we inoculated immunocompetent BALB/cByJ mice with a myeloma cell line - MOPC315.BM -, inducing a MM phenotype. Upon tumor establishment, characterization of the BM microenvironment revealed the expression of both activation and suppressive markers by lymphocytes, such as Granzyme b and PD-1, respectively. In addition, conditioning of the animals with MOPC315.BM-derived EV, before transplantation of the MOPC315.BM tumor cells, did not anticipate the disease phenotype. However, it induced features of suppression in the BM milieu, such as an increase in PD-1 expression by CD4+ T cells. Overall, our findings reveal the involvement of MOPC315.BM-derived EV protein content as promoters of immune niche remodeling, strengthening the importance of assessing the mechanisms by which MM may impact the immune microenvironment.

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