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MEOX2-mediated regulation of Cathepsin S promotes cell proliferation and motility in glioma.

ABSTRACT: MEOX2-mediated regulation of Cathepsin S promotes cell proliferation and motility in glioma.

PROVIDER: PRJNA812002 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18191900_1.fastq.gz	Fastqsanger.gz
	SRR18191900_2.fastq.gz	Fastqsanger.gz
	SRR18191901_1.fastq.gz	Fastqsanger.gz
	SRR18191901_2.fastq.gz	Fastqsanger.gz
	SRR18191902_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

MEOX2-mediated regulation of Cathepsin S promotes cell proliferation and motility in glioma.

Project description:Nuclear transcription factor Mesenchyme Homeobox 2 (MEOX2) is a homeobox gene that is originally discovered to suppress the growth of vascular smooth muscle and endothelial cells. However, whether or not it is connected to cancer is yet unknown. Here, we report that MEOX2 functions as a tumor-initiating element in glioma. Bioinformatic analyses of public databases and investigation of MEOX2 expression in patients with glioma demonstrated that MEOX2 was abundant at both mRNA and protein levels in glioma. MEOX2 expression was shown to be inversely linked with the prognosis of glioma patients. MEOX2 inhibition changed the morphology of glioma cells, inhibited cell proliferation and motility, whereas had no effect on cell apoptosis. Besides, silencing of MEOX2 also hampered the epithelial-mesenchymal transition (EMT), focal adhesion maturation, and F-actin assembly. Overexpression of MEOX2 exhibited opposite effects. Importantly, RNA-seq, ChIP assay, and luciferase reporter assay revealed Cathepsin S (CTSS) as a novel transcriptional target of MEOX2 in glioma cells. Consistently, MEOX2 causes glioma tumor development in mice and greatly lowers the survival period of tumor-bearing mice. Our findings indicate that MEOX2 promotes tumorigenesis and progression of glioma partially through the regulation of CTSS. Targeting the MEOX2-CTSS axis might be a promising alternative for the treatment of glioma.

2022-04-01 | GSE197758 | GEO

MEOX2 homeobox gene promotes growth of malignant gliomas [RNA-Seq]

Project description:Glioblastoma (GBM) is an aggressive tumor that frequently exhibits gain of chromosome 7, loss of chromosome 10 and aberrantly activated RTK signaling pathways. Here, we identify mesenchymal homeobox 2 (MEOX2) as a salient oncogenic transcription factor candidate with increased expression in GBMs. Our results suggest that MEOX2 can enhance ERK signaling through a feed-forward mechanism. We show that MEOX2 overexpression can lead to increased growth in bona fide GBM implantation models and cooperates with loss of p53 and PTEN in cerebral organoid models of human malignant gliomas to induce cell proliferation. Furthermore, using high-throughput genomics, we identify transcriptional target genes of MEOX2 in patient-derived GBM tumorsphere models and a fresh frozen GBM tumor.

2022-07-01 | GSE181144 | GEO

MEOX2 homeobox gene promotes growth of malignant gliomas [ACT-Seq & CUT&TAG]

2022-07-01 | GSE181145 | GEO

Multi-comparative Bioinformatic Detection of MEOX2 De Novo Motif Sites And Distal Intergenic Sequences By ChIP-Seq, Reveals MEOX2-Dependent Modulation of EGFR-Gene Sequences In A Lung Cancer Preclinical Model

Project description:Mesenchyme Homebox-2 (MEOX2) transcription factor and its role in lung malignant diseases. It is mentioned that MEOX2 has recently been proposed as a genetically amplified and overexpressed lung tumor biomarker that promotes cellular proliferation, tumor growth, pre- and clinical progression, and oncological therapy resistance. The study used a large-scale epigenome occupancy strategy to identify novel MEOX2-related cellular pathways. It was also discovered that MEOX2 has a significant occupation on distal intergenic sequences, De Novo Moitf Sites as well as on EGFR-genetic sequences, and positively regulates EGFR-gene expression in human lung cancer cells and preclinical tumor growth. The study concluded that overexpressed MEOX2 is negatively clinically correlated with poorer progression-free survival in lung cancer patients with early clinical stages, with or without EGFR-TKIs based therapy.

2023-06-15 | GSE230567 | GEO

Effect of Cathepsin L exposure on endothelial cell transcriptomics

Project description:Cathepsin L is a lysosomal protease that is secreted by several cancer cells. Cathepsin L upregulation has been widely associated with poor clinical outcome and increased metastatic incidence. However, whether Cathepsin L participates in tumor angiogenesis remains less studied. Our study showed a significant activation of angiogenic capacity of endothelial cells in presence of purified or tumor derived Cathepsin L. In addition, Cathepsin L exposure led to a significant increase in the proliferative capacity of endothelial cells. While the ability of Cathepsin L to promote endothelial cell sprouting, migration, invasion and tube formation can be attributed to its proteolytic effects on extracellular matrix, how it promotes endothelial cell proliferation remains obscure. The objective of this study was to test if Cathepsin L exposure can activate signaling cascades and gene expression leading to proliferation of endothelial cells.

2016-06-20 | GSE75744 | GEO

Autocrine Motility Factor Modulates Proliferation Signaling Mediated By GPER

Project description:Autocrine Motility Factor Modulates Proliferation Signaling Mediated By GPER

| PRJNA471076 | ENA

Histone deacetylase inhibitors impair glioblastoma cell motility and proliferation

Project description:Histone deacetylase inhibitors impair glioblastoma cell motility and proliferation

| PRJNA789840 | ENA

MEOX2 Regulates Adipogenic Differentiation of Adipose-Derived Stromal Vascular Fractions through PI3K/AKT Signaling Pathway

Project description:The fat tail of sheep is an important organ that has evolved to adapt to extreme environmental conditions. Mesenchyme homeobox 2 (MEOX2) can inhibit adipogenic differentiation of stromal vascular fractions (SVFs) isolated from ovine tail adipose tissue. However, the underlying mechanism through which MEOX2 regulates ovine adipogenesis remains unclear. Therefore, this study aims to employ RNA sequencing (RNA-seq) to explore the downstream genes regulated by MEOX2 during the adipogenic differentiation of ovine SVFs. Based on RNA sequencing, several differentially expressed genes (DEGs) were identified in response to MEOX2 overexpression. The PI3K/AKT signaling pathway was significantly enriched in DEGs, indicating its importance in mediating fat accumulation regulated by MEOX2. Additionally, the PI3K/AKT signaling pathway activation was found to be crucial for ovine SVF adipogenic differentiation. Mechanistically, MEOX2 inhibited the PI3K/AKT pathway. These findings highlight the significance of the PI3K/AKT signaling pathway during ovine SVF adipogenic differentiation. Furthermore, they shed light on the involvement of MEOX2 in this differentiation via the PI3K/AKT pathway. Our findings provide novel insights into the critical role of MEOX2 as an adipogenetic differentiation regulator, potentially enhancing our understanding of ovine fat development and its regulatory processes.

2024-10-01 | GSE266851 | GEO

RNA-seq analysis of glioblastoma stem cells where MEOX2 expression was knocked down by shRNAs

Project description:The most widely accepted hypothesis about glioblastoma onset indicates glioblastoma stem-like cells (GSCs) as the cells of origin, also responsible for the high chemo- and radio-resistance of this tumor and of its recurrence. MEOX2 is a transcription factor overexpressed in glioblastoma, whose expression is negatively correlated to patients’ survival. Starting from our observation that MEOX2 expression is strongly enhanced in six GSC lines we tested, we performed shRNA-mediated knock-down experiments in two different GSC lines, and found that MEOX2 depletion inhibits their self-renewal and growth ability, and increases the apoptotic cell death. By a deep transcriptome analysis, we identified a core group of genes modulated in response to MEOX2 knock-down. Among these genes, the repressed ones are largely enriched in genes involved in the hypoxic response and in the glycolytic pathway, two strictly related pathways which contribute to the resistance of high grade gliomas to therapies.

2022-05-18 | GSE196141 | GEO

Cathepsin L Regulates Metabolic Networks Controlling Rapid Cell Growth and Proliferation

Project description:Rapidly proliferating cells reshape their metabolism to satisfy their ever-lasting need for building blocks. This phenomenon is exemplified in certain malignant conditions but also occurs during embryonic development, when cells rely heavily on glycolytic metabolism to exploit their metabolic intermediates for biosynthetic routes. How cells regulate this metabolic makeover is currently unknown. Here we report that loss of cathepsin L (CtsL) is associated with fast proliferation rate and enhanced glycolytic metabolism that depend on lactate dehydrogenase A (LDHA) activity. Furthermore, we show that CtsL inhibition led to increased LDHA expression, suggesting of a causal relationship between LDHA expression and function. In conclusion, we propose that CtsL regulate this metabolic circuit to keep cell division under check.

2019-05-06 | PXD011588 | Pride

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