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RNA sequencing analysis of TFCP2L1 overexpression in thyroid cancer cells

ABSTRACT: RNA sequencing analysis of TFCP2L1 overexpression in thyroid cancer cells

PROVIDER: PRJNA1061576 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27442822_1.fastq.gz	Fastqsanger.gz
	SRR27442822_2.fastq.gz	Fastqsanger.gz
	SRR27442823_1.fastq.gz	Fastqsanger.gz
	SRR27442823_2.fastq.gz	Fastqsanger.gz
	SRR27442824_1.fastq.gz	Fastqsanger.gz

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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.

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RNA sequencing analysis of SLC6A15 overexpression in papillary thyroid cancer cells

Project description:Solute Carrier Family 6 Member 15 (SLC6A15) has been found with dysregulated expression in several kinds of cancers. However, its expression pattern and biological functions in papillary thyroid cancer (PTC) remain unknown. To explore the role of SLC6A15 in PTC, transcription profiling analysis was performed in KTC1 cells with or without SLC6A15 overexpression.

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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 SLC6A15 overexpression in papillary thyroid cancer cells

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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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Effects of CRABP1 overexpression on thyroid cancer cell lines

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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

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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.

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