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A regulatory axis of YY1-PFKP promotes aggressive prostate tumorigenesis via potentiating tumor cell metabolism [ChIP-seq]

ABSTRACT: A regulatory axis of YY1-PFKP promotes aggressive prostate tumorigenesis via potentiating tumor cell metabolism [ChIP-seq]

PROVIDER: PRJNA643527 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12125855.fastq.gz	Fastqsanger.gz
	SRR12125856.fastq.gz	Fastqsanger.gz

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Similar Datasets

A regulatory axis of YY1-PFKP promotes aggressive prostate tumorigenesis via potentiating tumor cell metabolism [ChIP-seq]

Project description:Yin Yang 1 (YY1) acts as a transcription factor crucially involved in cell proliferation, differentiation and survival. We here report that YY1, through gene expression regulation, plays an important role in prostate tumorigenesis, notably in castration-resistant prostate cancer (CRPC) models. Specifically, we found that YY1 displays a significantly elevated level among primary samples from prostate cancer patients, relative to normal. Depletion of YY1 in multiple independent prostate cancer model systems dramatically reduced tumor cell growth in vitro and significantly delayed oncogenic progression in vivo. Using integrated analyses of chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing (RNA-seq), we further defined YY1-regulated cistrome, among which include a set of metabolism-related genes such as PFKP (Phosphofructokinase, Platelet isoform), a rate-limiting enzyme essential for glycolysis. Via both gene loss-of-function and rescue studies, we demonstrate that PFKP serves as a key downstream direct target of YY1, significantly contributing to YY1-enforced oncogenic phenotypes such as enhanced tumor cell glycolysis and prostate cancer growth. Lastly, we show that BRD4, a cofactor of YY1, is critically involved in YY1-mediated activation of metabolic genes in prostate cancer cells. Altogether, this study unveils an oncogenic axis of YY1/BRD4-PFKP in prostate cancer for potentiating more aggressive tumor characteristics, which shall shed light on targeted therapy.

2021-06-03 | GSE153639 | GEO

A regulatory axis of YY1-PFKP promotes aggressive prostate tumorigenesis via potentiating tumor cell metabolism [RNA-seq]

2021-06-03 | GSE153518 | GEO

A regulatory axis of YY1-PFKP promotes aggressive prostate tumorigenesis via potentiating tumor cell metabolism

Project description:A regulatory axis of YY1-PFKP promotes aggressive prostate tumorigenesis via potentiating tumor cell metabolism

| PRJNA643524 | ENA

A regulatory axis of YY1-PFKP promotes aggressive prostate tumorigenesis via potentiating tumor cell metabolism [RNA-seq]

Project description:A regulatory axis of YY1-PFKP promotes aggressive prostate tumorigenesis via potentiating tumor cell metabolism [RNA-seq]

| PRJNA643522 | ENA

A regulatory axis of YY1-PFKP promotes aggressive prostate tumorigenesis via potentiating tumor cell metabolism

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-03 | GSE153640 | GEO

Yin Yang 1 interacts with bromodomain-containing coactivators to promote tumorigenesis of advanced prostate cancer

Project description:Castration-resistant prostate cancer (CRPC) is a terminal disease and the molecular underpinnings of CRPC development need to be better understood in order to improve its treatments. Here, we report that a transcription factor Yin Yang 1 (YY1) is significantly overexpressed during prostate cancer progression. Functional and cistrome studies of YY1 uncover its roles in promoting prostate oncogenesis in vitro and in vivo, as well as sustaining tumor metabolism including the Warburg effect and mitochondria respiration. Additionally, our integrated genomics and interactome profiling in prostate tumor show that YY1 and bromodomain-containing proteins (BRD2/4) co-occupy a majority of gene-regulatory elements, coactivating downstream targets. Via gene loss-of-function and rescue studies, as well as mutagenesis of YY1-bound cis-elements, we unveil an oncogenic pathway in which YY1 directly binds and activates PFKP, a gene encoding the rate-limiting enzyme for glycolysis, significantly contributing to YY1-enforced Warburg effect and malignant growth. Altogether, this study supports a master regulator role for YY1 in prostate tumor and reveals a YY1:BRD2/4-PFKP axis operating in advanced prostate cancer with implications for therapy.

2021-06-03 | GSE164719 | GEO

Leishmania regulates host YY1: comparative proteomic analysis identifies infection modulated YY1 dependent proteinsLeishmania regulates host YY1: comparative proteomic analysis identifies infection modulated YY1 dependent proteins

Project description:The protein Yin-Yang 1 (YY1) is a ubiquitous multifunctional transcription factor. Interestingly, there are several cellular functions controlled by YY1 that could play a role in Leishmania pathogenesis. Leishmaniasis is a human disease caused by protozoan parasites of the genus Leishmania. This study examined the potential role of macrophage YY1 in promoting Leishmania intracellular survival. Knockdown of YY1 resulted in attenuated survival of Leishmania in infected macrophages, suggesting a role of YY1 in Leishmania persistence. Biochemical fractionation studies revealed Leishmania infection caused redistribution of YY1 to the cytoplasm from the nucleus where it is primarily located. Inhibition of nuclear transport by leptomycin B attenuates infection-mediated YY1 redistribution and reduces Leishmania survival. This suggests that Leishmania induces the translocation of YY1 from the nucleus to the cytoplasm of infected cells, where it may regulate host molecules to favour parasite survival. A label-free quantitative whole proteome approach showed that the expression of a large number of macrophage proteins was dependent on the YY1 level. Interestingly, several of these proteins were modulated in Leishmania-infected cells, revealing YY1-dependent host response and suggesting their potential role in Leishmania pathogenesis. Together, these findings identify YY1 as a novel and essential virulence factor by proxy that promotes Leishmania survival.

2025-03-14 | PXD059968 | Pride

Cistrome analysis of YY1 uncovers a regulatory axis of YY1:BRD2/4-PFKP during tumorigenesis of advanced prostate cancer.

Project description:Castration-resistant prostate cancer (CRPC) is a terminal disease and the molecular underpinnings of CRPC development need to be better understood in order to improve its treatment. Here, we report that a transcription factor Yin Yang 1 (YY1) is significantly overexpressed during prostate cancer progression. Functional and cistrome studies of YY1 uncover its roles in promoting prostate oncogenesis in vitro and in vivo, as well as sustaining tumor metabolism including the Warburg effect and mitochondria respiration. Additionally, our integrated genomics and interactome profiling in prostate tumor show that YY1 and bromodomain-containing proteins (BRD2/4) co-occupy a majority of gene-regulatory elements, coactivating downstream targets. Via gene loss-of-function and rescue studies and mutagenesis of YY1-bound cis-elements, we unveil an oncogenic pathway in which YY1 directly binds and activates PFKP, a gene encoding the rate-limiting enzyme for glycolysis, significantly contributing to the YY1-enforced Warburg effect and malignant growth. Altogether, this study supports a master regulator role for YY1 in prostate tumorigenesis and reveals a YY1:BRD2/4-PFKP axis operating in advanced prostate cancer with implications for therapy.

| S-EPMC8136773 | biostudies-literature

Glycolytic Pfkp Acts as Lin41 Protein Kinase to Regulate Embryonic Stem Cell Differentiation

Project description:To investigate the synergistic role of Pfkp and Lin41 in the regulation of lineage differentiation, we knocked down Pfkp and Lin41 in mESC cells (R1 cells) by shRNAs respectively, and cultured for 6 days to form embryoid bodies (EBs).We then performed transcriptome sequencing of the Pfkp or Lin41 knockdown EBs.

2023-02-21 | GSE216394 | GEO

Effect of PFKP deletion on gene expression in laryngeal carcinoma cells LIU-LSC-1

Project description:To investigate the role of PFKP in laryngea cancer, we established a LIU-LSC-1 cell line with PFKP knocked down by lentivirus technique. We then performed gene expression profiling targeting the RNA-seq data of the control and PFKP knockdown groups.

2024-08-08 | GSE248242 | GEO

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