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Silencing of RNA binding protein, ZFP36L1, promotes epithelial-mesenchymal transition in liver cancer cells by regulating transcription factor ZEB2

ABSTRACT: Silencing of RNA binding protein, ZFP36L1, promotes epithelial-mesenchymal transition in liver cancer cells by regulating transcription factor ZEB2

PROVIDER: PRJNA672974 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12926426_1.fastq.gz	Fastqsanger.gz
	SRR12926426_2.fastq.gz	Fastqsanger.gz
	SRR12926428_1.fastq.gz	Fastqsanger.gz
	SRR12926428_2.fastq.gz	Fastqsanger.gz
	SRR12926429_1.fastq.gz	Fastqsanger.gz

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Silencing of RNA binding protein, ZFP36L1, promotes epithelial-mesenchymal transition in liver cancer cells by regulating transcription factor ZEB2

Project description:HCC cancer cells were knocked down of ZFP36L1 using siRNA and RNASeq was done.

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Project description:ZFP36L1 is a tandem zinc-finger RNA-binding protein that recognizes conserved Adenylate-Uridylate-rich Elements (AREs) located in 3' untranslated regions (UTRs) to mediate RNA decay. We hypothesized that ZFP36L1 is a negative regulator of a post-transcriptional hub involved in the RNA half-life regulation of cancer-related transcripts. Forced expression of ZFP36L1 in cancer cells markedly reduced cell proliferation in vitro and in vivo; whereas silencing of ZFP36L1 enhanced tumor cell growth. To identify direct downstream targets of ZFP36L1, systematic screening using RNA pull-down of wildtype and mutant ZFP36L1 as well as whole transcriptome sequencing of bladder cancer cells ± tet-on ZFP36L1, was performed. A network of 1,410 genes was identified as potential direct targets of ZFP36L1, including HIF1A, CCND1, and E2F1. ZFP36L1 specifically bound to the 3' UTRs of these targets for RNA degradation, thus suppressing their expression. Collectively, our findings reveal an indispensable role of ZFP36L1 as a post-transcriptional safeguard against aberrant hypoxic signaling and abnormal cell cycle progression.

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ZEB2, a master regulator of the epithelial-mesenchymal transition, mediates trophoblast differentiation

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ZEB2, a master regulator of the epithelial-mesenchymal transition, mediates trophoblast differentiation

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Transcriptome of ZFP36L1-sufficient and ZFP36L1-deficient Fo B cells

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ZEB2 protects the heart from ischemic damage

Project description:infarct size and subsequent deterioration in function. The identification of factors that enhance cardiac repair by the restoration of the vascular network is, therefore, of great significance. Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. Single-cell sequencing indicates ZEB2 to be enriched in injured cardiomyocytes. Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infarct healing post-myocardial infarction (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and cardiac function. We identified Thymosin 4 (TMSB4) and Prothymosin (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models. Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA, which enhances angiogenesis and prevents cardiac dysfunction. These findings reveal ZEB2 as a beneficial factor during ischemic injury, which may hold promise for the identification of new therapies.

2021-03-23 | PXD022212 | Pride

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