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Overexpressed Malat1 drives metastasis through inflammatory reprogramming of lung adenocarcinoma microenvironment

ABSTRACT: Overexpressed Malat1 drives metastasis through inflammatory reprogramming of lung adenocarcinoma microenvironment

PROVIDER: PRJNA1106755 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28859388.fastq.gz	Fastqsanger.gz
	SRR28859389.fastq.gz	Fastqsanger.gz
	SRR28859390.fastq.gz	Fastqsanger.gz
	SRR28859391.fastq.gz	Fastqsanger.gz
	SRR28859392.fastq.gz	Fastqsanger.gz

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Overexpressed Malat1 drives metastasis through inflammatory reprogramming of lung adenocarcinoma microenvironment

Project description:Although the expression of some long noncoding RNAs (lncRNAs), including MALAT1 (metastasis-associated lung adenocarcinoma transcript 1), is predictive of metastasis, their impact and mechanism of action remain elusive. Here we use CRISPR activation (CRISPRa) to model MALAT1/Malat1 overexpression in patient-derived lung adenocarcinoma (LUAD) cell lines and in the autochthonous K-ras/p53 LUAD mouse model. The results indicate that Malat1 overexpression alone is sufficient to enable the progression of LUAD to metastatic disease. We show that overexpressed MALAT1/Malat1 enhances cell mobility and promotes the recruitment of pro-tumor macrophages to the tumor microenvironment through paracrine secretion of the CCL2/Ccl2 cytokine. We determine that Ccl2 upregulation results from an increase in global chromatin accessibility upon Malat1 overexpression. Importantly, macrophage depletion and Ccl2 blockade counteracted the effects of Malat1 overexpression. These data demonstrate that a single lncRNA can drive LUAD metastasis through reprogramming of the tumor microenvironment.

2024-05-08 | GSE266561 | GEO

Overexpressed Malat1 drives metastasis through inflammatory reprogramming of lung adenocarcinoma microenvironment

2024-10-26 | GSE266323 | GEO

Overexpressed Malat1 drives metastasis through inflammatory reprogramming of lung adenocarcinoma microenvironment

Project description:Overexpressed Malat1 drives metastasis through inflammatory reprogramming of lung adenocarcinoma microenvironment

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Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment

2024-10-23 | GSE265872 | GEO

MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) Human HCC proteomics

Project description:The long noncoding RNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1), also known as MALAT-1 or NEAT2 (nuclear-enriched abundant transcript 2), is a highly conserved nuclear noncoding RNA (ncRNA). Two molecular functions of MALAT1 have been proposed, one is the control of alternative splicing and the other is the transcriptional regulation. To uncover its function in HCC, we knock down it in human HCC LM3 cell lines, and profiling the sample with LC/MS/MS and RNA sequencing.

2021-09-21 | PXD016790 | Pride

Differentiation of Mammary Tumors and Reduction in Metastasis Upon Malat1 LncRNA Loss

Project description:Genome-wide analyses have identified thousands of long non-coding RNAs (lncRNAs). Malat1 (Metastasis Associated Lung Adenocarcinoma Transcript 1) is among the most abundant lncRNAs whose expression is altered in numerous cancers. Here we report that genomic loss, as well as systemic knockdown of Malat1 using antisense oligonucleotides, in the MMTV-PyMT mouse mammary carcinoma model results in slower tumor growth accompanied by differentiation into highly cystic tumors and a significant reduction in lung metastasis. Further, Malat1 loss results in a reduction of branching morphogenesis in MMTV-PyMT and Her2/neu amplified tumor organoids consistent with the in vivo reduction in lung metastasis. At the molecular level, Malat1 knockdown results in alterations in gene expression and changes in splicing patterns of genes involved in differentiation and pro-tumorigenic signaling pathways. Together, these data indicate that the lncRNA Malat1 regulates critical processes in mammary cancer pathogenesis and represents a promising therapeutic target for inhibiting breast cancer metastasis. Transcriptome profiles of tumors and organoids after Malat1 knockdown using antisense olgonucleotides (ASOs).

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lncRNA MALAT1 interactome - Quantitative proteomics reveals that long non-coding RNA MALAT1 interacts with DBC1 to regulate p53 acetylation

Project description:Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA (lncRNA) that was first discovered as a prognostic marker for lung cancer metastasis. MALAT1 has been implicated in the tumorigenesis of numerous tumor types. To further delineate the underlying molecular mechanism, we established a high-throughput strategy to characterize the interacting proteins of MALAT1 by combining RNA pull down, quantitative proteomics, bioinformatics analysis, and experimental validation.

2018-10-26 | PXD005154 | Pride

Differentiation of Mammary Tumors and Reduction in Metastasis Upon Malat1 LncRNA Loss

2016-01-12 | GSE67647 | GEO

Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment

Project description:Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment

| PRJNA1104596 | ENA

Comparison of metastasis-inclined microenvironment (MIM) and metastasis-averse microenvironment (MAM) HCC patients

Project description:To determine the role of the hepatic microenvironment in HCC metastasis, we compared the gene expression profiles of 20 noncancerous surrounding hepatic tissues from two HCC patient groups, those with primary HCC together with venous metastasis which we termed a metastasis-inclined microenvironment (MIM) and those with HCC without detectable metastasis, which we termed a metastasis-averse microenvironment (MAM). There were a total of 20 cDNA microarrays performed, comparing 9 MIM or 11 MAM HCC patient samples to a common reference pool of 8 normal liver tissues.

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