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The Deubiquitylase USP52 Regulates Cell Proliferation and Ferroptosis through Stabilizing SLC7A11/xCT in Bladder Cancer

ABSTRACT: The Deubiquitylase USP52 Regulates Cell Proliferation and Ferroptosis through Stabilizing SLC7A11/xCT in Bladder Cancer

PROVIDER: PRJNA1095871 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28539772_1.fastq.gz	Fastqsanger.gz
	SRR28539772_2.fastq.gz	Fastqsanger.gz
	SRR28539773_1.fastq.gz	Fastqsanger.gz
	SRR28539773_2.fastq.gz	Fastqsanger.gz
	SRR28539774_1.fastq.gz	Fastqsanger.gz

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The Deubiquitylase USP52 Regulates Cell Proliferation and Ferroptosis through Stabilizing SLC7A11/xCT in Bladder Cancer

Project description:Ferroptosis, a recently coined non-apoptotic form of cell death, is triggered by lethal accumulation of iron-dependent lipid peroxidation. SLC7A11/xCT, acts as a central hub in ferroptosis, is closely related to the development of multiple human diseases. However, the specific functions and potential regulatory mechanisms of ferroptosis, especially xCT protein, in bladder cancer (BLCA) remain poorly understood. Herein, through an unbiased siRNA screen targeting 96 deubiquitinases (DUBs), we identified USP52/PAN2 as a top regulator essential for xCT protein translational activity and ferroptosis process. Functionally, loss of USP52 inhibits glutathione (GSH) synthesis through xCT degradation, leading to elevated lipid peroxidation and ferroptosis, thereby suppresses BLCA progression. Mechanistically, USP52 physically interacts with xCT through its WD40 domain, biochemically hydrolyzes the K48-conjugated ubiquitin chains of xCT at K4 and K12, thereby promotes its protein stability. Importantly, USP52 expression demonstrates a positive correlation with xCT expression in clinical BLCA samples, and high USP52 expression is linked to a worse progression and prognosis. Additionally, USP52 depletion and IKE synergistically restrained the progression of BLCA by triggering ferroptosis in vivo. Collectively, our findings reveal a molecular mechanism of USP52-xCT axis in ferroptosis, and uncover a previously unappreciated role of USP52 in BLCA tumorigenesis.

2024-12-09 | GSE263111 | GEO

Deubiquitylase USP52 Promotes Bladder Cancer Progression by Modulating Ferroptosis through Stabilizing SLC7A11/xCT.

Project description: Not available

| S-EPMC11615784 | biostudies-literature

ATF4 suppresses hepatocarcinogenesis by inducing SLC7A11 (xCT) to suppress stress-related ferroptosis

Project description:ATF4 suppresses hepatocarcinogenesis by inducing SLC7A11 (xCT) to suppress stress-related ferroptosis

| PRJNA789791 | ENA

SLC7A11 deficiency exacerbates systemic lupus erythematosus by inducing instability and ferroptosis in regulatory T cells

Project description:The amino acid transporter SLC7A11 (also known as xCT) mediates cystine uptake and plays a key role in maintaining cellular redox balance. Its function in regulatory T (Treg) cells remains incompletely understood.

2026-05-12 | GSE330183 | GEO

PGK1 acts as a non-catalytic gatekeeper of ferroptosis by stabilizing SLC7A11

Project description:Ferroptosis is restrained by layered antioxidant defenses, yet whether glycolytic enzymes directly constitute ferroptosis-defense machinery remains unclear. Here we identify phosphoglycerate kinase 1 (PGK1) as a non-canonical suppressor of ferroptosis that functions independently of its glycolytic kinase activity. Across pan-cancer bulk and single-cell transcriptomes, glycolysis inversely associates with ferroptosis programs, with PGK1 emerging as a prognostic hub. PGK1 loss in multiple tumor models elicits hallmark ferroptotic features, elevates lipid peroxidation and labile iron, and suppresses xenograft growth, all of which are reversed by liproxstatin-1. Mechanistically, PGK1 physically binds the C-terminal tail of SLC7A11 (aa 471-501) and shields it from ubiquitin-proteasome degradation, thereby sustaining cystine-driven glutathione synthesis and redox homeostasis. This scaffolding role is preserved in a kinase-dead PGK1 mutant, establishing a strict separation between metabolic and ferroptosis-regulatory functions. Restoring SLC7A11 rescues PGK1-deficient tumor growth, whereas a rationally designed competing peptide SLC7A11471-501 (FP-01) disrupts the PGK1-SLC7A11 interface, depletes SLC7A11/GSH, triggers ferroptosis, and suppresses tumor progression in vivo. Collectively, the PGK1-SLC7A11 interaction represents a druggable ferroptosis vulnerability that enables selective ferroptosis induction while sparing essential glycolysis.

2026-07-12 | GSE317428 | GEO

PGK1 acts as a non-catalytic gatekeeper of ferroptosis by stabilizing SLC7A11

Project description:PGK1 acts as a non-catalytic gatekeeper of ferroptosis by stabilizing SLC7A11

| PRJNA1412666 | ENA

PGK1 acts as a non-catalytic gatekeeper of ferroptosis by stabilizing SLC7A11 [RNA-Seq]

2026-07-13 | GSE338472 | GEO

The Deubiquitylase OTUB1 Mediates Ferroptosis via Stabilization of SLC7A11.

Project description: Not available

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PGK1 acts as a non-catalytic gatekeeper of ferroptosis by stabilizing SLC7A11 [scRNA-seq]

Project description:PGK1 acts as a non-catalytic gatekeeper of ferroptosis by stabilizing SLC7A11 [scRNA-seq]

| PRJNA1415234 | ENA

LncRNA SLC7A11-AS1 suppresses ferroptosis in hepatocellular carcinoma to promote tumorigenesis

Project description:LncRNAs are playing essential roles in epigenetic regulation, mRNA translation, and protein modification. However, the function of SLC7A11-AS1, an antisense lncRNA derived from the solute carrier family 7 member 11 (SLC7A11) gene, remains incompletely known. In this study, we utilized shRNA technology to knock down SLC7A11-AS1 in HepG2 cells, aiming to investigate the role of SLC7A11-AS1 in hepatocellular carcinoma. RNA-seq results revealed that there were 2536 differentially expressed genes upon SLC7A11-AS1 knockdown.

2024-07-17 | GSE244762 | GEO

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