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Role of Forkhead Box P3 in Interferon g-mediated PD-L1 Expression and Bladder Cancer Differentiation

ABSTRACT: Role of Forkhead Box P3 in Interferon g-mediated PD-L1 Expression and Bladder Cancer Differentiation

PROVIDER: PRJNA1115527 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29149977_1.fastq.gz	Fastqsanger.gz
	SRR29149977_2.fastq.gz	Fastqsanger.gz
	SRR29149978_1.fastq.gz	Fastqsanger.gz
	SRR29149978_2.fastq.gz	Fastqsanger.gz
	SRR29149979_1.fastq.gz	Fastqsanger.gz

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Role of Forkhead Box P3 in Interferon g-mediated PD-L1 Expression and Bladder Cancer Differentiation

Project description:Antagonism of the PD-1/PD-L1 axis is a critical therapeutic strategy for advanced bladder cancer patients. IFNg functions as a key regulator of PD-L1 in both immune as well as cancer cells. Forkhead Box P3 (FOXP3) is a transcription factor synonymous in T regulatory cell function, but with increasingly described functions in cancer cells. Here we investigated the relationship between FOXP3 and PD-L1 in bladder cancer. We showed that FOXP3 is critical in the ability for IFNg to activate PD-L1 in bladder cancer cells. FOXP3 can bind to the PD-L1 promoter and induces a gene program that leads to regulation of multiple immune-related genes and genes involved in epithelial-to-mesenchymal transition. Using in vitro and in vivo human and murine models, we showed that FOXP3 can regulate bladder cancer differentiation as well as promote metastases. Furthermore, FOXP3 may be a convergent factor for multiple activators of PD-L1 including by cisplatin.

2024-10-09 | GSE268243 | GEO

Role of Forkhead Box P3 in IFNγ-Mediated PD-L1 Expression and Bladder Cancer Epithelial-to-Mesenchymal Transition.

Project description:Antagonism of the PD-1/PD-L1 axis is a critical therapeutic strategy for patients with advanced bladder cancer. IFNγ functions as a key regulator of PD-L1 in both immune as well as cancer cells. Forkhead box P3 (FOXP3) is a transcription factor synonymous in T regulatory cell function but with increasingly described functions in cancer cells. Here, we investigated the relationship between FOXP3 and PD-L1 in bladder cancer. We showed that FOXP3 is critical in the ability for IFNγ to activate PD-L1 in bladder cancer cells. FOXP3 can bind to the PD-L1 promoter and induces a gene program that leads to regulation of multiple immune-related genes and genes involved in epithelial-to-mesenchymal transition (EMT). Using in vitro and in vivo human and murine models, we showed that FOXP3 can influence bladder cancer EMT as well as promote cancer metastases. Furthermore, FOXP3 may be a convergent factor for multiple activators of PD-L1, including the chemotherapeutic drug cisplatin.SignificanceHistorically a key transcription factor driving T regulatory cell function, FOXP3 has an increasingly recognized role in cancer cells. In bladder cancer, we defined a novel mechanism whereby FOXP3 mediates the activation of the immune checkpoint PD-L1 by the cytokine IFNγ. We also showed that FOXP3 induces other immune checkpoints as well as genes involved in EMT, promoting immune resistance and cancer metastases.

| S-EPMC11345674 | biostudies-literature

Effect of forkhead box M1 in multiple myeloma

Project description:Effect of forkhead box M1 in multiple myeloma

| PRJNA746277 | ENA

Forkhead Box F1 acts as a novel prognostic biomarker and induces caspase-dependent apoptosis in bladder cancer

Project description:Forkhead Box F1 acts as a novel prognostic biomarker and induces caspase-dependent apoptosis in bladder cancer

| PRJNA956253 | ENA

Forkhead box E1 (FOXE1) RNAis vs control RNAi in HEKa cells

Project description:Analysis of HEKa cells depleted of Forkhead box E1 (FOXE1). FOXE1 is induced in psoriasis lesions and promotes keratinocytes. Results provide insight into the downstream targets of FOXE1 function in psoriasis.

2021-01-09 | GSE164438 | GEO

Forkhead Box F1 acts as a novel prognostic biomarker and induces caspase-dependent apoptosis in bladder cancer

Project description:Down-regulated expression of Forkhead Box F1 (FOXF1) in malignant tumors were reported in several kinds of cancer before, but its role in bladder cancer (BC) was not clear. This study aims to demonstrate the prognostic value and of FOXF1 in BC patients. Here, a retrospectively recruited BC cohort and public datasets were utilized to identify the predictive ability of FOXF1 and its relationship between clinical information in BC patients. The expression level of FOXF1 is notably higher in BC tissues than para-cancerous mucosae. Low FOXF1 expression is correlated to unfavorable clinicopathological features and poor prognosis. Further, in bladder tumor cells, the expression levels of FOXF1 mRNA and protein were tested by quantitative real-time PCR and western blot. The viability of cells was examined by CCK-8, EdU, and clonogenic capacity assays. Cell apoptosis was detected by flow cytometry. We note that FOXF1 activating could impair cell viability and induce apoptosis in BC. Then, caspase 3 as a downstream gene of FOXF1 was spotted by RNA-Seq and PPI. The anti-tumor effect of FOXF1 were also validated in animal models. In conclusion, down-regulated FOXF1 expression is a potential independent indicator for unfavorable clinical outcomes of BC patients, FOXF1 inhibits BC cells proliferation and induces cell apoptosis via caspase signaling pathway. This study exhibits FOXF1 express pattern, demonstrates the prognostic predictive ability of FOXF1 and prove the anti-tumor mechanisms of FOXF1 in BC, it has reference value to clinical decision, activation FOXF1 expression could be used as a new strategy in tumor therapeutics.

2023-07-18 | GSE229810 | GEO

Forkhead box Q1-regulated transcriptome in human breast cancer cells

Project description:Forkhead box Q1-regulated transcriptome in human breast cancer cells

| PRJNA634524 | ENA

Forkhead box F1 overexpression initiates Barrett’s like metaplasia by promoting trans-differentiation and wound repair

Project description:The forkhead box (FOX) family of transcriptional regulators is characterized by a distinct forkhead DNA-binding domain11. FOXF1 gene is highly conserved across species and implicated in embryonic digestive tract morphogenesis. In an in-vitro established model, normal esophageal squamous cells, EPC2, were transfected with FOXF1 to determine pathways regulated by FOXF1 during the squamous to columnar change in cells.

2021-11-12 | GSE122481 | GEO

Identification of a forkhead box protein transcriptional network induced in human neutrophils in response to inflammatory stimuli

Project description:We performed the first RNAseq analysis of human primary neutrophils exposed to lipopolysaccharide which revealed a robustly enhanced transcriptional network driven by forkhead box (FOX) transcription factors.

2023-01-02 | GSE221866 | GEO

Forkhead Box Protein P3 (FOXP3) Represses ATF3 Transcriptional Activity.

Project description:Activating transcription factor 3 (ATF3), a transcription factor and acute stress sensor, is rapidly induced by a variety of pathophysiological signals and is essential in the complex processes in cellular stress response. FOXP3, a well-known breast and prostate tumor suppressor from the X chromosome, is a novel transcriptional repressor for several oncogenes. However, it remains unknown whether ATF3 is the target protein of FOXP3. Herein, we demonstrate that ATF3 expression is regulated by FOXP3. Firstly, we observed that overexpression of FOXP3 reduced ATF3 protein level. Moreover, knockdown FOXP3 by siRNA increased ATF3 expression. Secondly, FOXP3 dose-dependently reduced ATF3 promoter activity in the luciferase reporter assay. Since FOXP3 is regulated by post-translational modifications (PTMs), we next investigated whether PTMs affect FOXP3-mediated ATF3 expression. Interestingly, we observed that phosphorylation mutation on FOXP3 (Y342F) significantly abolished FOXP3-mediated ATF3 expression. However, other PTM mutations on FOXP3, including S418 phosphorylation, K263 acetylation and ubiquitination, and K268 acetylation and ubiquitination, did not alter FOXP3-mediated ATF3 expression. Finally, the FOXP3 binding site was found on ATF3 promoter region by deletion and mutagenesis analysis. Taken together, our results suggest that FOXP3 functions as a novel regulator of ATF3 and that this novel event may be involved in tumor development and progression.

| S-EPMC8583784 | biostudies-literature

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