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Targeting the mRNA endonuclease CPSF73 inhibits breast cancer cell migration and invasion

ABSTRACT: Targeting the mRNA endonuclease CPSF73 inhibits breast cancer cell migration and invasion

PROVIDER: PRJNA784305 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17055836_1.fastq.gz	Fastqsanger.gz
	SRR17055836_2.fastq.gz	Fastqsanger.gz
	SRR17055837_1.fastq.gz	Fastqsanger.gz
	SRR17055837_2.fastq.gz	Fastqsanger.gz
	SRR17055838_1.fastq.gz	Fastqsanger.gz

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Targeting the mRNA endonuclease CPSF73 inhibits breast cancer cell migration and invasion

Project description:Targeting the mRNA endonuclease CPSF73 inhibits breast cancer cell migration and invasion

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Targeting the mRNA endonuclease CPSF73 inhibits breast cancer cell migration and invasion

Project description:Cleavage by the endonuclease CPSF73 and polyadenylation of nascent RNA is an essential step in co-transcriptional mRNA maturation, and abnormal poly(A) site choices have been associated with human diseases, including cancer. Recent work has surprisingly identified CPSF73 as a promising drug target for inhibiting the growth of specific cancers. However, our understanding of the regulation of CPSF73 is still at an early stage. Here, we report that a HECT-like E3 ligase, UBE3D, participates in stabilizing CPFS73 protein by preventing its ubiquitin-mediated degradation by the proteasome. Depletion of UBE3D in both non-cancer cells and cancer cells leads to CPSF73 downregulation, a pre-mRNA cleavage defect and dysregulated gene expression. UBE3D dysfunction or chemical inactivation of CPFS73 inhibited migration and invasion as well as stem cell renewal phenotypes in vitro in triple negative breast cancer cells. Our findings indicate that targeting the pre-mRNA processing nuclease CPSF73 has potential for breast cancer therapy.

2021-12-05 | GSE189723 | GEO

Targeting the mRNA endonuclease CPSF73 inhibits breast cancer cell migration and invasion

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Project description:Metastasis accounts for almost 90% of breast cancer-related fatalities, making it frequent malignancy and the main reason of tumor mortality globally among women. A key player in breast cancer is the histone demethylase lysine-specific demethylase 1 (LSD1). We used LSD1 knockdown MCF7 and T47D cell exosomes to treat breast cancer cells for greatly increasing the invasion and migration of breast cancer cells for evaluating the impact of LSD1 on breast cancer invasion and migration. miR-1290 expression was downregulated in LSD1 knockdown MCF7 exosomes. Furthermore, miR-1290 could control NAT1 expression by looking through the database of miR-1290 target genes. These data provide fresh insights into the biology of breast cancer therapy by demonstrating how the epigenetic factor LSD1 stimulates the breast cancer cells’ invasion and migration via controlling exosomal miRNA.

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