RAD18 promotes cell malignant behaviors of esophageal squamous cell carcinoma by modulating ATM/STAT3/PD-L1.

Xianghui Yang, Qishi Song, Min Li, Da Liu

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Article in Chromosoma, 2025. 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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5 · Who and what money

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4 authors.

Xianghui YangDepartment of Oncology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha City, Hunan Province, China. yangxianghui_yxh@163.com.

Qishi SongDepartment of Oncology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha City, Hunan Province, China.

Min LiInterventional Treatment Room, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha City, Hunan Province, China.

Da LiuDepartment of Respiratory and Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha City, Hunan Province, China.

Funding

Changsha Natural Science Foundation Project No. kq2208447

6 · The paper itself

Abstract

backgroundEsophageal cancer (EC) is still a difficult problem in medicine, depriving many patients of their lives every year. RAD18 and ATM were implicated in cancers including esophageal squamous cell carcinoma (ESCC). However, whether RAD18/ATM axis influences ESCC progression remains unclear.

methodsThe abundance of genes and proteins was evaluated using RT-qPCR and western blot. Cell proliferation, migration and invasion were examined using clone formation, scratch test and transwell. The level of ATM ubiquitination was verified and experimented using Co-IP.

resultsOur findings found that RAD18 expression was enhanced in TCGA database, in ESCC patients and ESCC cells. Similarly, ATM expression was declined in ESCC patients and ESCC cells. RAD18 silencing resulted in suppression of cell proliferation, migration and invasion of ESCC cells, which were abolished by ATM silencing. In addition, ATM silencing promoted malignant behaviors of ESCC cells by activating STAT3/PD-L1 axis, which was reversed by PD-L1 knockdown. Moreover, RAD18 could reduce ATM protein levels.

conclusionRAD18 mediated ATM ubiquitination to reduce ATM protein level, thereby activating STAT3/PD-L1 axis and strengthening cell proliferation, migration and invasion of ESCC cells.

Indexed as

Ataxia Telangiectasia Mutated ProteinsB7-H1 AntigenDNA-Binding ProteinsEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaSTAT3 Transcription FactorUbiquitin-Protein LigasesCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansSignal TransductionUbiquitinationAtaxia Telangiectasia Mutated ProteinsATM protein, humanB7-H1 AntigenCD274 protein, humanDNA-Binding ProteinsRAD18 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorUbiquitin-Protein LigasesATMESCCRAD18STAT3/PD-L1 axisUbiquitination

Identifiers

PMID40632228

DOI10.1016/j.canlet.2017.12.034

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