SUMOylation controls Hu antigen R posttranscriptional activity in liver cancer

The posttranslational modification of proteins critically influences many biological processes and is a key mechanism that regulates the function of the RNA-binding protein Hu antigen R (HuR), a hub in liver cancer. Here, we show that HuR is SUMOylated in the tumor sections of patients with hepatoce...

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Detalles Bibliográficos
Autores: Lachiondo Ortega, Sofia, Rejano Gordillo, Claudia M., Simon, Jorge, Lopitz Otsoa, Fernando, C. Delgado, Teresa, Mazan Mamczarz, Krystyna, Goikoetxea Usandizaga, Naroa, Velázquez Cruz, Alejandro, Díaz Quintana, Antonio Jesús, Díaz Moreno, Irene, Martínez-Chantar, María Luz
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2024
País:España
Institución:Universidad de Sevilla (US)
Repositorio:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/160902
Acceso en línea:https://hdl.handle.net/11441/160902
https://doi.org/10.1016/j.celrep.2024.113924
Access Level:acceso abierto
Palabra clave:CP: Cancer
CP: Molecular biology
ELAVL1
HCC
PTMs
Senescence
SUMO
Descripción
Sumario:The posttranslational modification of proteins critically influences many biological processes and is a key mechanism that regulates the function of the RNA-binding protein Hu antigen R (HuR), a hub in liver cancer. Here, we show that HuR is SUMOylated in the tumor sections of patients with hepatocellular carcinoma in contrast to the surrounding tissue, as well as in human cell line and mouse models of the disease. SUMOylation of HuR promotes major cancer hallmarks, namely proliferation and invasion, whereas the absence of HuR SUMOylation results in a senescent phenotype with dysfunctional mitochondria and endoplasmic reticulum. Mechanistically, SUMOylation induces a structural rearrangement of the RNA recognition motifs that modulates HuR binding affinity to its target RNAs, further modifying the transcriptomic profile toward hepatic tumor progression. Overall, SUMOylation constitutes a mechanism of HuR regulation that could be potentially exploited as a therapeutic strategy for liver cancer.