ArticleNature communications2026
Mutant TP53 hijacks RNA-splicing factor RBM28 to suppress double-stranded RNA triggered antitumor immunity.
Tao Xiang, Ziyi He, Xiao Hu, Xiaoyuan Wang, Shaosen Zhang, Shihao Zhu, Jie Yang, Hanzhang Yi, Qingyi Liu, Wen Tan and 2 more
Abstract read
In one paragraphArticle in Nature communications, 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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5 · Who and what moneyAuthors and funding
12 authors.
Tao Xiang *Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Ziyi He *Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Xiao Hu *Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Xiaoyuan Wang *Department of Thoracic Surgery, Harbin Medical University Cancer Hospital, Harbin, China.ORCID 0009-0007-0381-827X Shaosen ZhangDepartment of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Shihao ZhuDepartment of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Jie YangDepartment of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Hanzhang YiDepartment of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Qingyi LiuDepartment of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0001-1313-8418 Wen TanDepartment of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-7231-7838 Dongxin LinDepartment of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. lindx@cicams.ac.cn.ORCID 0000-0002-8723-8868 Chen WuDepartment of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. chenwu@cicams.ac.cn.ORCID 0000-0003-4954-1011 Funding
No grant is acknowledged in the PubMed record.
6 · The paper itselfAbstract
TP53 mutation may not only compromise its multifaceted tumor-suppressive functions but also confer oncogenic properties. Here, we demonstrate that DNA-binding domain mutations of TP53 unexpectedly confer a transcriptional regulatory function, directly driving RNA-splicing factor RBM28 overexpression. Overexpressed RBM28 excessively splices transposon elements, inhibiting double-stranded RNA (dsRNA) formation, thereby suppressing dsRNA-triggered type I interferon (IFN) signaling and subsequent anti-tumor immunity. We demonstrate in mouse tumorigenesis models and human multi-stage esophageal cancer development that mutant p53 (mutp53)-driven aberrant RBM28/dsRNA/IFN axis plays a crucial role in cancer initiation, progression and resistance to immune checkpoint blockade (ICB) therapy through innate immune suppression. Pan-cancer analysis indicates that this mechanism underlies ICB resistance in most cancers. Pharmacological restoration of normal p53 conformation or targeted RNA-splicing inhibition enhances anti-tumor immunity and ICB efficacy. Collectively, our study has unveiled an important function of mutp53 in establishing immunosuppressive tumor microenvironment, which provides an actionable framework for intervention and therapy in TP53-mutated cancers.
Indexed as
RNA-Binding ProteinsRNA, Double-StrandedTumor Suppressor Protein p53AnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansImmunity, InnateInterferon Type IMiceMutationRNA SplicingTumor MicroenvironmentInterferon Type IRNA-Binding ProteinsRNA, Double-StrandedTP53 protein, humanTumor Suppressor Protein p53
Identifiers
PMID42778550
PMCPMC13601520
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