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High-throughput sequencing identified differentially expressed RNAs between MALAT1 knockdown C3H10 adipocyte and control cells

ABSTRACT: High-throughput sequencing identified differentially expressed RNAs between MALAT1 knockdown C3H10 adipocyte and control cells

PROVIDER: PRJNA658520 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12491805_1.fastq.gz	Fastqsanger.gz
	SRR12491805_2.fastq.gz	Fastqsanger.gz
	SRR12491806_1.fastq.gz	Fastqsanger.gz
	SRR12491806_2.fastq.gz	Fastqsanger.gz

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High-throughput sequencing identified differentially expressed RNAs between MALAT1 knockdown C3H10 adipocyte and control cells

Project description:Although MALAT1 is a lncRNA highly expressed in many tissues and participates in a series of physiological and pathological processes, the potential role of MALAT1 in adipogenesis is not clear. To gain full insights into MALAT1 function in the adipogenic differention of C3H10 cell, we performed RNA-seq to antisense oligonucleotides(ASO) treated C3H10 cells and found numerous differentially expressed RNAs between MALAT1 knockdown C3H10 adipocyte and control cells.

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Project description:Previously, lncRNA Malat1 knockout mice were generated by insertional inactivation. By crossing this line to MMTV-PyMT mammary tumor mouse model, we produced PyMT;Malat1 wild-type (WT) and PyMT;Malat1 knockout (KO). Furthermore, we generated Malat1 transgenic mice by targeting ROSA26 locus and bred them to PyMT;Malat1 knockout mice to produce Malat1-rescued PyMT;Malat1 knockout;Malat1 transgenic animals (TG). Using mammary tumors from the three groups of animals, we performed RNA-Seq analysis to identify differentially up-regulated genes in KO tumors to find novel target genes of YAP-TEAD pathway.

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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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