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Divergent roles of KLF4 and TFCP2L1 in ground-state naive pluripotency and human primordial germ cell development

ABSTRACT: Divergent roles of KLF4 and TFCP2L1 in ground-state naive pluripotency and human primordial germ cell development

PROVIDER: PRJNA625486 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11549068.fastq.gz	Fastqsanger.gz
	SRR11549069.fastq.gz	Fastqsanger.gz
	SRR11549070.fastq.gz	Fastqsanger.gz
	SRR11549071.fastq.gz	Fastqsanger.gz
	SRR11549072.fastq.gz	Fastqsanger.gz

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Divergent roles of KLF4 and TFCP2L1 in ground-state naive pluripotency and human primordial germ cell development

Project description:During development, human primordial germ cells (hPGCs) transition through a transcriptional and epigenetic state similar to pre-implantation epiblast cells called naive ground-state pluripotency. Diagnostic transcription factors that define this state include TFAP2C, KLF4, and TFCP2L1, with TFAP2C necessary for both establishment of the naive-like state in hPGC-like cells (hPGCLCs) as well as establishment and self-renewal of naive human embryonic stem cells (hESCs). Here, we show that KLF4 and TFCP2L1 are not required for hPGC specification or establishment of the naive-like state in hPGCLCs. Instead, KLF4 and TFCP2L1 are each required for reversion of primed hESCs to the self-renewing naive ground state. Additionally, TFCP2L1 but not KLF4 function after hPGC specification in the proliferation of the hPGCLC population.

2022-04-30 | GSE148717 | GEO

Resetting Transcription Factor Control Circuitry Towards Ground State Pluripotency In Human

Project description:Current human pluripotent stem cells lack the transcription factor circuitry that governs the ground state of mouse embryonic stem cells (ESC). Here we report that short-term expression of two components, NANOG and KLF2, is sufficient to ignite other elements of the network and reset the human pluripotent state. Inhibition of ERK and protein kinase C signalling sustains a transgene-independent rewired state. Reset cells self-renew continuously without ERK signalling, are phenotypically stable and karyotypically intact. They differentiate in vitro and form teratomas in vivo. Metabolism is reprogrammed in reset cells with activation of mitochondrial respiration as in ESC. DNA methylation is dramatically reduced and transcriptome state is globally realigned across multiple cell lines. Depletion of ground state transcription factors, TFCP2L1 or KLF4 has marginal impact on conventional human pluripotent stem cells, but collapses the reset state. These findings demonstrate feasibility of installing and propagating functional control circuitry for ground state pluripotency in human cells. DNA methylation analysis in Conventional and Reset human embryonic stem cells by whole genome bisulfite sequencing, in triplicate, using the Illumina platform

2014-09-10 | E-GEOD-60945 | biostudies-arrayexpress

Resetting Transcription Factor Control Circuitry Towards Ground State Pluripotency In Human

2014-09-10 | GSE60945 | GEO

Identification of CDK1 phosphorylation of TFCP2L1 from murine embryonic stem cells and bladder cancer cells

Project description:Molecular programs involved in embryogenesis are frequently upregulated in oncogenic dedifferentiation and metastasis. However, their precise roles and regulatory mechanisms remain elusive. Here, we showed that CDK1 phosphorylation of TFCP2L1, a pluripotency-associated transcription factor, orchestrated pluripotency and cell-cycling in embryonic stem cells (ESCs) and was aberrantly activated in aggressive bladder cancers (BCs). In murine ESCs, the protein interactome and transcription targets of Tfcp2l1 indicated its involvement in cell-cycle regulation. Tfcp2l1 was phosphorylated at Thr177 by Cdk1, which affected ESC cell-cycle progression, pluripotency, and differentiation. LC-MS was used to characterize thr177 phosphorylation in TFCP2L1 protein obtained by IP experiment and kinase assay. The CDK1-TFCP2L1 pathway was activated in human BC cells, stimulating their proliferation, self-renewal, and invasion. Lack of TFCP2L1 phosphorylation impaired the tumorigenic potency of BC cells in a xenograft model. In patients with BC, high co-expression of TFCP2L1 and CDK1 was associated with unfavorable clinical characteristics including tumor grade, lymphovascular and muscularis propria invasion, and distant metastasis and was an independent prognostic factor for cancer specific survival. These findings demonstrate the molecular and clinical significance of CDK1-mediated TFCP2L1 phosphorylation in stem-cell pluripotency and in the tumorigenic stemness features associated with BC progression.

2019-11-08 | PXD015635 | Pride

RNA sequencing analysis of TFCP2L1 overexpression in thyroid cancer cells

Project description:To investigate the genes and pathways regulated by TFCP2L1 in thyroid cancer cells, we established TFCP2L1-overexpressing TPC1 cell line and performed RNA sequencing for further study.

2024-05-22 | GSE252658 | GEO

Tfcp2l1 controls cellular patterning of the collecting duct.

Project description:Gene expression analysis of mouse kidney after conditional inactivation of transcription factor Tfcp2l1

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Identify Tfcp2l1-regulated genes in mouse embryonic stem cells grown in 2i medium

Project description:Mouse embryonic stem cells (ESCs) grown in the 2i (an ERK inhibitor, PD0325901, and a GSK-3b inhibitor, CHIR99021) mimic pluripotent epiblasts in preimplantation blastocysts. ESCs grown in FBS containing medium are more heterogenous in morphology and expression of stem cell factors. Tfcp2l1 is a transcription factor highly expressed in ESCs grown in the 2i medium, suggesting that it plays in important role in ESC biology. To search for the putative role(s) of Tfcp2l1 in ESCs, we plan to use an integrated genomic approach--combing RNA-seq and ChIP-seq--to identify the direct targets of Tfcp2l1 in ESCs. RNA-seq is used to identify the transcripts regulated by Tfcp2l1 in ESCs grown in the 2i medium.

2021-03-01 | GSE159937 | GEO

Identify genomic binding sites of Tfcp2l1 in mouse embryonic stem cells grown in 2i medium

Project description:Mouse embryonic stem cells (ESCs) grown in the 2i (an ERK inhibitor, PD0325901, and a GSK-3b inhibitor, CHIR99021) mimic pluripotent epiblasts in preimplantation blastocysts. Tfcp2l1 is a transcription factor highly expressed in ESCs grown in the 2i medium, suggesting that it plays in important role in ESC biology. To search for the putative role(s) of Tfcp2l1 in ESCs, we plan to use an integrated genomic approach--combing RNA-seq and ChIP-seq--to identify the direct targets of Tfcp2l1 in ESCs. ChIP-seq is used to identify the genomic bindings sites of Tfcp2l1 in ESCs grown in the 2i medium.

2021-03-01 | GSE159877 | GEO

TFCP2L1 promotes GPX4-mediated ferroptosis to inhibit breast cancer cell proliferation and metastasis via the PI3K/AKT signaling pathway

Project description:Breast cancer represents the most prevalent form of malignant tumors among women. Despite the existence of numerous therapeutic methods, a significant portion of patients face a poor prognosis, highlighting the urgency in identifying new remedial targets. Here, we for the first time demonstrated that the CP2 family member TFCP2L1, a classical marker of embryonic stem cell maintenance, as a tumor suppressor in breast cancer. Patients with breast cancer have poorer prognoses when TFCP2L1 is expressed highly. Consistently, the expression of TFCP2L1 is higher in normal breast cells than those in breast cancer cell lines. Gain- and loss-of-function and xenograft tumor assay showed that overexpression of TFCP2L1 significantly inhibited both the proliferation and migration of breast cancer cells in vivo and in vitro. Conversely, the knockdown of TFCP2L1 promoted the proliferation and migration of breast cancer cells. Mechanistically, we found that TFCP2L1 suppresses breast cancer progression by directly inhibiting the expression of glutathione peroxidase 4 (GPX4), a key regulator of ferroptosis. Therefore, inhibition of GPX4 by RSL3, an inducer of ferroptosis was able to promote the function of TFCP2L1 in breast cancer cells. On the other hand, transcriptome high-throughput exhibited that TFCP2L1 negatively regulated the activity of PI3K/AKT signaling pathway. Administration of SC79, an AKT activator, was capable of partially restoring the negative effects of TFCP2L1 on GPX4 transcription. Together, TFCP2L1 functions by directly or indirectly regulating GPX4-mediated ferroptosis, and may serve as a novel biomarker and potential therapeutic target for breast cancer.

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Genome wide map of Tfcp2l1 binding sites from mouse kidney

Project description:We identified Tfcp2l1 binding sites in mouse kidney using Chromatin Immunoprecipitation followed by high-throughput sequencing (ChiP-Seq)

2017-06-19 | GSE87752 | GEO

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