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Lnc RNA FENDRR attenuates adriamycin resistance via suppressing MDR 1 expression through sponging HuR and miR‐184 in chronic myelogenous leukaemia cells
Author(s) -
Zhang Feng,
Ni Haiwei,
Li Xiaoman,
Liu Hai,
Xi Tao,
Zheng Lufeng
Publication year - 2019
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13480
Subject(s) - multiple drug resistance , apoptosis , cancer research , microrna , rna , in vitro , downregulation and upregulation , chemistry , biology , microbiology and biotechnology , pharmacology , drug resistance , biochemistry , gene
Chemotherapy is a major anticancer therapeutic modality, however, multidrug resistance ( MDR ) is frequently observed and hinders treatment efficacy. Here, we investigated the role and potential mechanism of the long noncoding RNA (lnc RNA ) F ENDRR in adriamycin resistance of chronic myeloid leukaemia ( CML ) cells. FENDRR overexpression attenuates adriamycin resistance, as shown by increased Rhodamine 123 accumulation, promotion of cell apoptosis in vitro and suppression of tumour growth in vivo . Mechanistically, we identified that FENDRR reduces the interaction of the RNA ‐binding protein HuR with MDR 1 via acting as a sponge, and miR‐184 competitively binds to FENDRR with HuR. Thus, the HuR/ FENDRR /miR‐184 interaction contributes to MDR 1 activity. These findings indicate that FENDRR is a potential target for reversing adriamycin resistance.