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Original Articles

Let-7b regulates the adriamycin resistance of chronic myelogenous leukemia by targeting AURKB in K562/ADM cells

ORCID Icon, , , , , , , , & show all
Pages 3451-3459 | Received 10 Feb 2020, Accepted 07 Aug 2020, Published online: 28 Aug 2020
 

Abstract

Chronic myeloid leukemia (CML) is a malignant hematological disease, and drug resistance is often related to poor prognosis. MicroRNAs (miRNA) play a pivotal role in transcriptional regulation, cell development, and chemotherapy resistance. Here, we describe the effect of let-7b on resistant leukemia cells and examine the relevance of let-7b as a biomarker for adriamycin resistance. Results showed that let-7b was downregulated in K562/ADM (KA) cells, and the downregulation of let-7b in K562 and KA cells increased ADM resistance. The inhibition of let-7b subsequently induced the upregulation of AURKB. Finally, results proved that the Pi3k/Akt/Erk pathway was related to AURKB-activated resistance. Our research indicated that the underexpression of let-7b and overexpression of AURKB contributed to the resistance of CML, and its function is partly regulated by the Pi3k/Akt/Erk pathway. Thus, our further understand of its inhibitory effect may promise a new therapeutic strategy to overcome chemotherapeutic resistance in CML.

Disclosure statement

The authors declare no competing interests.

Additional information

Funding

This work was supported by the National Natural Science Foundation of China under Grant 81800169, 81772281; Shandong Science and Technology Committee under Grant 2018GSF118056, ZR2019MH022; Foundation of Shandong Educational Committee under Grant J17KA121, 2019KJK014; Yantai Science and Technology Committee under Grant 2018XSCC051; and Shandong Province Taishan Scholar Project under Grant ts201712067.

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