Evidence map›Paper›PMID 41832622›Full record

ArticleEndocrine, metabolic & immune disorders drug targets2026

UBE2M Identified by CRISPR Screening as a Key Regulator of Cisplatin-Induced Acute Kidney Injury via the p53 Pathway

Cheng Yuan, Feng Chen, Xueyun Gao, Ayinigaer Yusufu, Danqin Lu, Xiaoyan Wu, Lihua Ni

Abstract read
In one paragraph

Article in Endocrine, metabolic & immune disorders drug targets, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Cheng YuanDepartment of Oncology, Yichang Central People's Hospital and The First College of Clinical Medical Science, China Three Gorges University, Yichang, Hubei, China.ORCID 0000-0002-0226-614X
Feng ChenDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, China.ORCID 0009-0006-4714-8477
Xueyun GaoDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, China.ORCID 0009-0004-7204-1087
Ayinigaer YusufuDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, China.ORCID 0009-0006-6248-3134
Danqin LuDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, China.ORCID 0009-0001-9016-5268
Xiaoyan WuDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, China.
Lihua NiDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, China.ORCID 0000-0002-0456-3279

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAcute kidney injury caused by cisplatin (Cis-AKI) is a major limitation in its clinical use, primarily due to the lack of effective therapeutic targets to mitigate nephrotoxicity. Although several molecular pathways are involved in Cis-AKI, identifying reliable and actionable therapeutic targets has been challenging. Through a CRISPR-based genome-wide screening approach, UBE2M was identified as a novel gene involved in cellular survival during cisplatin-induced stress. However, its expression, biological function, and underlying mechanism in Cis-AKI have not been thoroughly investigated. This study aims to identify key therapeutic targets for Cis- AKI and investigate the role of UBE2M in this condition.

methodsA CRISPR-Cas9 genome-wide screening approach was employed to identify key genes involved in cisplatin-induced renal tubular epithelial cell injury. UBE2M, identified as a critical survival factor, was further investigated using both gain- and loss-of-function strategies to explore its biological function and underlying regulatory mechanisms in the Cis-AKI model.

resultsCRISPR screening identified UBE2M as a key regulator of cellular survival in Cis-AKI, and subsequent validation experiments confirmed its suppression in cisplatin-induced renal injury models. UBE2M overexpression alleviated apoptosis and renal injury by reducing p53 activation. In contrast, UBE2M knockdown exacerbated these effects, leading to increased apoptosis and renal injury. DISCUSSION: This study reveals that UBE2M is a critical regulator of cisplatin-induced renal tubular epithelial cell injury. By regulating the p53-mediated apoptotic pathway, UBE2M protects against Cis-AKI.

conclusionUBE2M could serve as a novel therapeutic target for the prevention and treatment of cisplatin-induced nephrotoxicity.

Indexed as

Acute Kidney InjuryAntineoplastic AgentsCisplatinClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsTumor Suppressor Protein p53Ubiquitin-Conjugating EnzymesAnimalsApoptosisHumansMiceSignal TransductionAntineoplastic AgentsCisplatinTrp53 protein, mouseTumor Suppressor Protein p53Ubiquitin-Conjugating Enzymesacute kidney injury (AKI)apoptosisCisplatinp53renal tubular epithelial cells.UBE2M

Identifiers

PMID41832622
PMCPMC13284637

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