Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cyclosporin A inhibits prostate cancer growth through suppression of E2F8

ABSTRACT: Cyclosporin A inhibits prostate cancer growth through suppression of E2F8

PROVIDER: PRJNA431263 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Cyclosporin A inhibits prostate cancer growth through suppression of E2F8

Project description:Cyclosporin A (CsA) is a potent immunosuppressive agent used clinically in organ transplantation. In this study, we examined that CsA exerts anti-tumor activity against prostate cancer. We performed microarray experiments to investigate the effect of CsA on the transcriptome of prostate cancer cells. CsA potently induced transcriptome change and primarily affected cell cycle-related gene signatures. These results suggest that CsA can be used as a potential therapeutic agent or an intriguing tool for exploring prostate cancer biology and identifying novel therapeutic targets.

2023-10-04 | GSE109505 | GEO

Cyclosporin A inhibits prostate cancer growth through suppression of E2F8 transcription factor in a MELK‑dependent manner.

Project description:The treatment of advanced prostate cancer remains a formidable challenge due to the limited availability of effective treatment options. Therefore, it is imperative to identify promising druggable targets that provide substantial clinical benefits and to develop effective treatment strategies to overcome therapeutic resistance. Cyclosporin A (CsA) showed an anticancer effect on prostate cancer in cultured cell and xenograft models. E2F8 was identified as a master transcription factor that regulated a clinically significant CsA specific gene signature. The expression of E2F8 increased during prostate cancer progression and high levels of E2F8 expression are associated with a poor prognosis in patients with prostate cancer. MELK was identified as a crucial upstream regulator of E2F8 expression through the transcriptional regulatory network and Bayesian network analyses. Knockdown of E2F8 or MELK inhibited cell growth and colony formation in prostate cancer cells. High expression levels of E2F8 and androgen receptor (AR) are associated with a worse prognosis in patients with prostate cancer compared with low levels of both genes. The inhibition of E2F8 improved the response to AR blockade therapy. These results suggested that CsA has potential as an effective anticancer treatment for prostate cancer, while also revealing the oncogenic role of E2F8 and its association with clinical outcomes in prostate cancer. These results provided valuable insight into the development of therapeutic and diagnostic approaches for prostate cancer.

| S-EPMC10636720 | biostudies-literature

Characterization of E2F8-mediated transcriptional regulation in lethal prostate cancer

Project description:To identify the genomic bindings and transcriptional targets of E2F8 in lethal prostate cancer cells. To examine the potential off-target effects by CRISPR/CasRx-mediated E2F8 knockdown in 293FT cells. To analyze differentially expressed genes upon TT3 LLN-CRISPR/CasRx-mediated E2F8 knockdown in DU145 xenografts.

2025-01-10 | GSE275631 | GEO

Suppression of CCT3 inhibits tumor growth by downregulating CDK1 expression in melanoma

Project description:Suppression of CCT3 inhibits tumor growth by downregulating CDK1 expression in melanoma

| PRJNA604922 | ENA

Murine Back Skin: Control vs. Cyclosporin A-treated

Project description:We analyzed the gene expression at the onset of hair growth induced by cyclosporin A (CsA), a well-known hair growth inducer, with DNA microarray, and unveiled the step-by-step progression of hair growth. KEYWORDS: Cyclosporin A, Cyclosporine A, Ciclosporin A

2009-12-24 | GSE16739 | GEO

Renal Cyclosporin-A (CsA) toxicity

Project description:Renal Cyclosporin-A (CsA) toxicity

| PRJNA437288 | ENA

Targeting AXL inhibits the growth and metastasis of prostate cancer in bone

Project description:We evaluated soluble AXL (sAXL or batiraxcept), a decoy receptor that can potently inhibit AXL signaling, as a single agent or in combination with docetaxel or carboplatin to treat prostate cancer (PCa) bone metastases. We used intratibial injection of multiple patient-derived xenografts with different characteristics, reflecting a traditional phase II clinical trial without pre-selection for a particular tumor characteristic. Inhibition of tyrosine kinase receptor AXL was highly effective as a single agent and showed additive effects when combined with docetaxel or carboplatin in suppressing PCa tumor growth in the bone and in suppressing metastasis to the lung. AXL inhibition suppressed critical cancer stem cell gene expression and significantly decreased proliferation and metastasis through suppression of E2F1 and NuSAP1. Our findings provide compelling preclinical data for testing batiraxcept in patients with prostate cancer with bone metastases.

2025-01-23 | GSE281461 | GEO

Targeting AXL inhibits the growth and metastasis of prostate cancer in bone

Project description:Targeting AXL inhibits the growth and metastasis of prostate cancer in bone

| PRJNA1183887 | ENA

Suppression of ANGPTL4 Reprograms Endothelial Cell Metabolism and Inhibits Angiogenesis

Project description:Suppression of ANGPTL4 Reprograms Endothelial Cell Metabolism and Inhibits Angiogenesis

| PRJNA869060 | ENA

Targeted suppression of ZNF217-induced AKT signaling inhibits tumor growth and metastasis in osteosarcoma

Project description:Targeted suppression of ZNF217-induced AKT signaling inhibits tumor growth and metastasis in osteosarcoma

| PRJNA614505 | ENA