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ZNF252P promotes tumorigenesis by activating c-Myc-mediated positive feedback loop

ABSTRACT: ZNF252P promotes tumorigenesis by activating c-Myc-mediated positive feedback loop

PROVIDER: PRJNA1132162 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29713575_1.fastq.gz	Fastqsanger.gz
	SRR29713575_2.fastq.gz	Fastqsanger.gz
	SRR29713576_1.fastq.gz	Fastqsanger.gz
	SRR29713576_2.fastq.gz	Fastqsanger.gz
	SRR29713577_1.fastq.gz	Fastqsanger.gz

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ZNF252P promotes tumorigenesis by activating c-Myc-mediated positive feedback loop

Project description:Here we screened and identified a novel oncogenic lncRNA, ZNF252P, which is upregulated in a variety of cancer types. ZNF252P promotes cancer cell proliferation and tumorigenicity in vitro and in vivo by activating c-Myc-mediated positive feedback loop. The pivotal regulatory axis of ZNF252P/c-Myc gives it the potential to be the promising biomarker and therapeutic target in cancer development.

2025-01-21 | GSE271524 | GEO

Global analysis of RNA-binding proteins identifies a positive feedback loop between LARP1 and MYC that promotes tumorigenesis

Project description:In addition to genomic alterations, aberrant changes in post-transcriptional regulation can modify gene function and drive cancer development. RNA-binding proteins (RBPs) are a large class of post-transcriptional regulators that have been increasingly implicated in carcinogenesis. By integrating multi-omics data, we identify LARP1 as one of the most upregulated RBPs in colorectal cancer (CRC), and demonstrate its oncogenic properties. We perform LARP1:RNA interactome profiling and unveil a previously unexplored role for LARP1 in targeting the 3′UTR of oncogenes in CRC. Notably, we identify the proto-oncogenic transcription factor MYC as a key LARP1-regulated target. Our data show that LARP1 positively modulates MYC expression by associating with its 3′UTR. In addition, antisense oligonucleotide-mediated blocking of the interaction between LARP1 and the MYC 3′UTR reduces MYC expression and in vitro CRC growth. Furthermore, a systematic analysis of LARP1:protein interactions reveals IGF2BP3 and YBX1 as LARP1-interacting proteins that also regulate MYC expression and CRC development. Finally, we demonstrate that MYC reciprocally modulates LARP1 expression by targeting its enhancer. In summary, our data reveal a critical, previously uncharacterized role of LARP1 in promoting CRC tumorigenesis, validate its direct regulation of the proto-oncogene MYC, and delineate a model of the positive feedback loop between MYC and LARP1 that promotes CRC growth and development.

2022-03-10 | PXD030215 | Pride

Analyses of RNAi-heterochromatin positive feedback loop in Tetrahymena

Project description:Analyses of RNAi-heterochromatin positive feedback loop in Tetrahymena

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A positive feedback loop controls Toxoplasma chronic differentiation

Project description:Successful infection strategies must balance pathogen amplification and persistence. In Toxoplasma gondii, this is accomplished through differentiation into dedicated cyst-forming chronic stages that avoid clearance by the host immune system. The transcription factor BFD1 is both necessary and sufficient for stage conversion; however, its regulation is not understood. We examine five factors transcriptionally activated by BFD1. One of these is a cytosolic RNA-binding protein of the CCCH-type zinc finger family, which we name BFD2. Parasites lacking BFD2 fail to induce BFD1 and are consequently unable to fully differentiate in culture or in mice. BFD2 interacts with the BFD1 transcript under stress and deletion of BFD2 reduces BFD1 protein levels, but not mRNA abundance. The reciprocal effects on BFD2 transcription and BFD1 translation outline a positive feedback loop that enforces commitment to differentiation. BFD2 helps explain how parasites commit to the chronic gene-expression program and elucidates how the balance between proliferation and persistence is achieved over the course of infection.

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A positive feedback loop mediates crosstalk between calcium, cyclic nucleotide and lipid signaling in Toxoplasma gondii.

Project description:Fundamental processes of obligate intracellular parasites, such as Plasmodium falciparum and Toxoplasma gondii are controlled by a set of plant-like calcium dependent kinases (CDPKs), the conserved cAMP- and cGMP-dependent protein kinases (PKA and PKG), second messengers and lipid signalling. While some major components of the signalling networks have been identified, how these are connected is largely not known. Here, we compare the phospho-signalling networks during Toxoplasma egress from its host cell by artificially raising cGMP or calcium levels to activate PKG or CDPKs, respectively. We show that both these inducers trigger near identical signalling pathways and provide evidence for a feedback loop involving CDPK3. We measure phospho- and lipid signalling in parasites treated with the Ca2+ ionophore A23187 in a sub-minute timecourse and show CDPK3-dependent regulation of diacylglycerol levels and increased phosphorylation of four phosphodiesterases (PDEs), suggesting their function in the feedback loop. Disruption of CDPK3 leads to elevated cAMP levels and inhibition of PKA signalling rescues the egress defect of ΔCDPK3 parasites treated with A23187. Biochemical analysis of the four PDEs identifies PDE2 as the only cAMP-specific PDE among these candidates while the other PDEs are cGMP specific; two of which are inhibited by the predicted PDE inhibitor BIPPO. Conditional deletion of the 4 PDEs supports an important, but non-essential role of PDE1 and PDE2 for growth, while only the latter plays a role in controlling A23187-mediated egress. In summary, we uncover a positive feedback loop that potentiates signalling during egress and links several signalling pathways together.

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Project description:The oncoprotein c-Myc is a key transcription factor with essential functions in the nucleolus (NO) to regulate ribosomal RNA (rRNA) synthesis, ribosome biogenesis, and cell proliferation. Yet, the mechanism that regulates the distribution and function of nucleolar c-Myc is still not completely understood. In this study, we identified nucleolar protein ENBA1 binding protein 2 (EBP2) as a novel functional binding partner of c-Myc. We found that coexpression of EBP2 markedly relocalized c-Myc from the nucleus to the NO, whereas depletion of EBP2 reduced the nucleolar distribution of c-Myc. Further study indicated that EBP2 is a direct binding partner of c-Myc and can block the degradation of c-Myc in a FBW7 (F-box and WD repeat domain containing 7)-independent manner. Moreover, EBP2 is a transcriptional target of c-Myc. c-Myc can bind to the promoter of EBP2 and positively regulate the EBP2 expression. Both protein and mRNA levels of EBP2 are upregulated in lung cancer samples and positively correlated with c-Myc expression. Functionally, EBP2 promotes c-Myc-mediated rRNA synthesis and cell proliferation. Collectively, our study indicates that EBP2 is a novel binding partner of c-Myc that regulates the function of nucleolar c-Myc, cell proliferation, and tumorigenesis via a positive feedback loop.

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Analyses of scnRNAs in the mutatnts defective in an RNAi-heterochromatin positive feedback loop in Tetrahymena [scnRNA]

Project description:In the ciliated protozoan Tetrahymena, an RNAi-mediated feedback loop is important for assembling heterochromatin on the sequences that are removed from the somatic genome by programmed DNA elimination. Because heterochromatin is formed exclusively on the eliminated sequences, some mechanism must inhibit this feedback loop at the boundaries of the eliminated sequences. In this study, we show that the HP1-like protein Coi6p, its interaction partners Coi7p and Lia5p, and the histone demethylase Jmj1p are crucial for confining the production of small RNAs to the eliminated sequences.

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The wound activated ERF15 transcription factor drives Marchantia polymorpha regeneration by activating an oxylipin biosynthesis feedback loop

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Analyses of heterochromatin distributions in the mutatnts defective in an RNAi-heterochromatin positive feedback loop in Tetrahymena [ChIP]

Project description:In the ciliated protozoan Tetrahymena, an RNAi-mediated feedback loop is important for assembling heterochromatin on the sequences that are removed from the somatic genome by programmed DNA elimination. Because heterochromatin is formed exclusively on the eliminated sequences, some mechanism must inhibit this feedback loop at the boundaries of the eliminated sequences. In this study, we show that the HP1-like protein Coi6p, its interaction partners Coi7p and Lia5p, and the histone demethylase Jmj1p are crucial for confining the formation of heterochromatin to the eliminated sequences.

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