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RNA-seq Analysis of the effect of Tfcp2l1 overexpression on Human ESC maintenace

ABSTRACT: RNA-seq Analysis of the effect of Tfcp2l1 overexpression on Human ESC maintenace

PROVIDER: PRJNA473659 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7233672.fastq.gz	Fastqsanger.gz
	SRR7233673.fastq.gz	Fastqsanger.gz

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RNA-seq Analysis of the effect of Tfcp2l1 overexpression on Human ESC maintenace

Project description:Purpose:The goals of this study are to analyze the candidate genes motified by Tfcp2l1 overexpression to regulated the human embryonic stem cell (ESC) self-renewal through RNA-seq approach.

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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

RNA-seq Analysis of the effect of Tfcp2l1 knockdown on Human ESC maintenace

Project description:Purpose:The goal of this study is to analyze the candidate genes motified byTfcp2l1 knockdown to regulated the human embryonic stem cell (ESC) fate through RNA-seq approach.

2017-08-23 | GSE102798 | 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:RNA sequencing analysis of TFCP2L1 overexpression in thyroid cancer cells

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RNA-Seq Gene Expression Analysis in Rat Metanephric Mesenchyme overexpressing Transcription Factor Tfcp2l1

Project description:We identified genes regulated by Tfcp2l1 overexpression in Rat Metanephric Mesenchyme

2017-06-19 | GSE87744 | 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

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

Hypoxia-induced expression of Tfcp2l1 promotes cell immortalization by enhancing cellular reprogramming

Project description:Cellular senescence is a stress response mechanism maintaining tissue homeostasis by changing physiological state and inducing irreversible proliferative arrest. It has been reported that hypoxia can bypass senescence and extend lifespan of naïve primary cells, mainly, by the decrease in oxidative damage. However, it is unclear how hypoxia can promote the evasion of senescence and promote cell immortalization prior to malignant transformation. We observed that the lifespan of MEFs is increased when they are cultured in hypoxia, reducing the expression of p16INK4a, p15INK4b and p21Cip1. In transcriptional genetic screenings, we found that proliferating naïve MEFs in hypoxia overexpress Tfcp2l1, which is a main regulator of pluripotency and self-renewal in embryonic stem cells, ESCs, as well as stemness-associated genes like Oct3/4, Sox2, Nanog. Tfcp2l1 expression is lost during culture in normoxia. The expression of Tfcp2l1 in hypoxia seems to be regulated by Hif1α and only when it is overexpressed at similar levels to those induced physiologically by hypoxia it increases lifespan of MEFs and promotes overexpression of stemness-associated genes. In Chip-seq experiments, we found that Tfcp2l1 binds and activate the expression of genes which regulate proliferation, which in many cases, are also related to stem cell properties, such as Sox2, Sox9 and Tgfa. Additionally, Tfcp2l1 can replicate the effect of hypoxia increasing cellular reprogramming and its expression correlates positively with the expression of Nanog and negatively with p21Cip1 and p16INK4a. Altogether, our data suggests that the activation of Tfcp2l1 by hypoxia could be relevant in the immortalization prior to malignant transformation, facilitating tumorigenesis and dedifferentiation of cells.

2024-02-22 | GSE173648 | 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.

2024-07-30 | GSE270578 | GEO

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