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ABSTRACT: 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

PROVIDER: PRJNA962546 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24324475_1.fastq.gz	Fastqsanger.gz
	SRR24324475_2.fastq.gz	Fastqsanger.gz

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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.

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Project description: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

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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.

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