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Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE119759 | GEO | 2018/11/01

REPOSITORIES: GEO

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Targeting FOXA1-mediated repression of TGF-? signaling suppresses castration-resistant prostate cancer progression.

Project description: Not available

| S-EPMC6355239 | biostudies-literature

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [microarray]

Project description:our study establishes FOXA1 as an important regulator of lineage plasticity mediated in part by TGF-β signaling and supports a novel therapeutic strategy to control lineage switching and potentially extend clinical response to antiandrogen therapies.

2018-11-01 | GSE119758 | GEO

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [RNA-Seq]

2018-11-01 | GSE119757 | GEO

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression

Project description:Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression

| PRJNA490185 | ENA

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [microarray]

Project description:Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [microarray]

| PRJNA490187 | ENA

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [RNA-Seq]

Project description:Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [RNA-Seq]

| PRJNA490188 | ENA

Targeting Galectin-1 Impairs Castration-Resistant Prostate Cancer Progression and Invasion.

Project description: Not available

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Oleocanthal Attenuates Metastatic Castration-Resistant Prostate Cancer Progression and Recurrence by Targeting SMYD2.

Project description: Not available

| S-EPMC9317016 | biostudies-literature

Targeting HIC1/TGF-β axis-shaped prostate cancer microenvironment restrains its progression.

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| S-EPMC9296670 | biostudies-literature

Targeting SOX4/PCK2 signaling suppresses neuroendocrine differentiation of castration-resistant prostate cancer

Project description:Background: Neuroendocrine prostate cancer (NEPC), a lethal subset of prostate cancer, is characterized by loss of AR signaling and resulting resistance to AR-targeted therapy during neuroendocrine transdifferentiation, for which the molecular mechanisms remain unclear. Here, we report that SRY-Box transcription factor 4 (SOX4) is upregulated in NEPC, which induces neuroendocrine markers, neuroendocrine cell morphology, and NEPC cell aggressive behavior. Methods: To understand the function of SOX4 in the development and progression of NEPC, we detected malignancy characterization after over-expression or knock-down of SOX4 in prostate cancer cells. Xenograft tumors representing NEPC subtypes were analyzed by pathologists. Protein expression profiles were validated in patient tumor tissue. Diagnoses were complemented by transcriptome sequencing and ATAC sequencing of specific cell lines and public clinical datasets. Results: SOX4 expression was significantly elevated in NEPC. Activating SOX4 in non-NEPC cells induced NE transdifferentiation, while silencing it in NEPC cells impeded NEPC progression. SOX4 promote neuroendocrine characteristics by inducing PCK2-mediated metabolism changing. Conclusions: Elevated SOX4 drives NE transdifferentiation in PCa via PCK2-mediated . Altogether, these findings highlight SOX4 as a novel molecule to drive NEPC progression and suggest that it might be a potential therapeutic target for NEPC.

2024-03-31 | GSE261370 | GEO

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