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miRNA-223-3p modulates ibrutinib resistance through regulating CHUK/NF-κB signaling pathway in mantle cell lymphoma.

Jingjing Yuan,Qing Zhang,Shengsheng Wu,Suran Yan,R. Zhao,Yajuan Sun,Xiaoxu Tian,K. Zhou

Published 2021 in Experimental Hematology

ABSTRACT

With the application of Brutons tyrosine kinase(BTK) inhibitor ibrutinib in relapsed / refractory (R/R) mantle cell lymphoma (MCL), the problem of drug resistance is increasingly prominent. Though non-classical nuclear factor kappa-B pathway (non-classical NF-κB pathway) has been proved to be correlated with ibrutinib resistance in MCL, the upstream regulator is unknown. In the present study, CHUK overexpression accelerated proliferation and suppressed apoptosis of MCL cells after ibrutinib treatment in vitro. The results of luciferase reporter assay, real-time quantitative PCR(RT-qPCR) and western blot showed that CHUK was targeted and negatively regulated by miRNA-223-3p. miRNA-223-3p knockdown promoted proliferation and inhibited apoptosis of MCL cells after ibrutinib treatment in vitro and vivo, whereas CHUK knockdown reversed down-regulated miRNA-223-3p-promoted cell proliferation after ibrutinib treatment in vitro. In conclusion, miRNA-223-3p modulates ibrutinib resistance through regulating CHUK/NF-κB signaling pathway in MCL, which is crucial to provide a marker to predict disease response.

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