APR-246 triggers ferritinophagy and ferroptosis of diffuse large B-cell lymphoma cells with distinct TP53 mutations View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2022-07-14

AUTHORS

Yuheng Hong, Tianyuan Ren, Xiaoxuan Wang, Xia Liu, Yue Fei, Shen Meng, Xu Han, Cong Sun, Hongru Shen, Lanfang Li, Lihua Qiu, Zhengzi Qian, Shiyong Zhou, Huilai Zhang, Xianhuo Wang

ABSTRACT

TP53 mutations correlate with inferior survival in many cancers. APR-246 is a compound to shift mutant p53 and exhibits anti-cancer effects. Among its effects, APR-246 facilitates the binding of restored p53 mutants to target genes and their transcription. A set of 2464 DLBCL cases from multiple cohorts including our center, was integrated to identify the type and localization of TP53 mutations and clinical impacts. APR-246 was applied in TP53-mutated DLBCL cells and xenograft mouse models to explore the anti-tumor effect. TP53 mutations frequency was 16% and TP53 mutations correlated with poor overall survival (OS) and progression-free survival (PFS) in all cases, especially in germinal center B-cell-like (GCB) and unclassified (UNC) subtypes. Notably, TP53 single mutations in the DNA binding domain (DBD) led to poor OS and PFS. Specifically, mutations in exon 7 correlated with poorer OS, while mutations in exons 5 and 6 associated with inferior PFS. APR-246 induces p53-dependent ferritinophagy of DLBCL cells with TP53 missense mutation on exon 7 and ferroptosis of DLBCL cells harboring wild-type TP53 and other TP53 mutations. TP53 mutations on exons 5, 6 and 7 are predictors of progression and survival. Targeting mutant p53 by APR-246 is a promising therapeutic approach for DLBCL patients. More... »

PAGES

2269-2280

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41375-022-01634-w

    DOI

    http://dx.doi.org/10.1038/s41375-022-01634-w

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1149468397

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/35835991


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