Ibrutinib targets microRNA-21 in multiple myeloma cells by inhibiting NF-κB and STAT3. Issue 1 (January 2018)

• Record Type: Journal Article
• Authors: Ma, Jing; Gong, Wei; Liu, Su; Li, Qian; Guo, Mengzheng; Wang, Jinhan; Wang, Suying; Chen, Naiyao; Wang, Yafei; Liu, Qiang; Zhao, Hui
• Is Part Of: Tumor biology. Volume 40:Issue 1(2018)
• Publication Date: 2018-01
• Subjects: Ibrutinib -- microRNA-21 -- multiple myeloma -- nuclear factor-κB -- signal transducer and activator of transcription 3; Cancer -- Periodicals; Oncology -- Periodicals; Tumors -- Periodicals; 616.994
• DOI: 10.1177/1010428317731369
• Languages: English
• ISSNs: 1010-4283

Abstract

The oncogenic microRNA-21 contributes to the pathogenesis of multiple myeloma. Ibrutinib (also referred to as PCI-32765), an inhibitor of Bruton's tyrosine kinase, while its effects on multiple myeloma have not been well described. Here, we show that microRNA-21 is an oncogenic marker closely linked with progression of multiple myeloma. Moreover, ibrutinib attenuates microRNA-21 expression in multiple myeloma cells by inhibiting nuclear factor-κB and signal transducer and activator of transcription 3 signaling pathways. Taken together, our results suggest that ibrutinib is a promising potential treatment for multiple myeloma. Further investigation of mechanisms of ibrutinib function in multiple myeloma will be necessary to evaluate its use as a novel multiple myeloma treatment.