Drug resistance-related microRNAs in hematological malignancies: Translating basic evidence into therapeutic strategies

Xie, Lingling; Jing, Rongrong; Qi, Jing; Lin, Zenghua; Ju, Songguang

doi:10.1016/j.blre.2014.09.005

Cited by 28 publications

(19 citation statements)

References 171 publications

(180 reference statements)

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“…As a class of regulatory small noncoding RNAs, microRNAs (miRNAs) are also widely involved in regulation of chemoresistance in malignancies . miRNAs interfere with coding messenger RNA (mRNA) translation in a sequence‐specific manner .…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐494 sensitizes colon cancer cells to fluorouracil through regulation of DPYD

et al. 2015

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Chemoresistance of colon cancer cells to the chemotherapeutics is still a main obstacle in treatment of this malignancy. The microRNA (miRNA) mediated chemosensitivity regulation in colon cancer cells is still largely unknown. Here we constructed a fluorouracil (5-Fu) resistant SW480 cell line (SW480/ 5-Fu) and discovered that miRNA miR-494 was downregulated in the drug resistant cells compared with the parental cells. miR-494 level was found to be correlated with 5-Fu sensitivity in colon cancer cells, and artificial alteration of miR-494 affects the sensitivity of colon cancer cell lines to 5-Fu. miR-494 also promoted apoptosis of colon cancer cells at present of 5-Fu. Importantly, as a regulatory enzyme in the 5-Fu catabolic pathway, DPYD was confirmed to be a direct target of miR-494 through the interaction of miR-494 and its binding site within DPYD 3 0 untranslated region (3 0 UTR). miR-494 also negatively regulated endogenous DPYD expression in SW480 cells. Overexpression or knockdown of DPYD could attenuate miR-494 mediated 5-Fu sensitivity regulation, suggesting the dependence of DPYD regulation in miR-494 activity. miR-494 inhibited SW480/5-Fu derived xenograft tumors growth in vivo at present of 5-Fu. Thus, we concluded that in colon cancer cells, tumor suppressor miR-494 enhanced 5-Fu sensitivity via regulation of DPYD expression. V C 2015 IUBMB Life, 67(3):191-201, 2015

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Section: Introductionmentioning

confidence: 99%

MicroRNA‐494 sensitizes colon cancer cells to fluorouracil through regulation of DPYD

et al. 2015

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“…Previous studies have found that many miRNAs are involved in drug resistance [21,22]. miR-130a can act as a tumour suppressor by targeting BCL2 and MCL-1 expression, lower expression of miR-130a is associated with poor prognosis in CML patients [23].…”

mentioning

confidence: 99%

LncRNA FENDRR attenuates adriamycin resistance via suppressing MDR1 expression through sponging HuR and miR‐184 in chronic myelogenous leukaemia cells

Zhang

Li³

et al. 2019

FEBS Letters

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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 (lncRNA) FENDRR 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 MDR1 via acting as a sponge, and miR‐184 competitively binds to FENDRR with HuR. Thus, the HuR/FENDRR/miR‐184 interaction contributes to MDR1 activity. These findings indicate that FENDRR is a potential target for reversing adriamycin resistance.

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“…Moreover, bioinformatics analysis predicted that CDC25B is a direct target of miR-27a, and the dual-luciferase reporter assay confirmed that CDC25B is a target gene of miR-27a. In many examples, the identification of a specific target of miRNA indicates important cellular events, and altered miRNA expression is a common feature of numerous diseases [22]. In addition, we found that the overexpression of miR-27a decreased the CDC25B mRNA and protein levels in K562 cells.…”

Section: Discussionmentioning

confidence: 48%

MiR-27a Promotes Hemin-Induced Erythroid Differentiation of K562 Cells by Targeting CDC25B

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNAs (miRNAs) play a crucial role in erythropoiesis. MiR-23a∼27a∼24-2 clusters have been proven to take part in erythropoiesis via some proteins. CDC25B (cell division control Cdc2 phosphostase B) is also the target of mir-27a; whether it regulates erythropoiesis and its mechanism are unknown. Methods: To evaluate the potential role of miR-27a during erythroid differentiation, we performed miR-27a gain- and loss-of-function experiments on hemin-induced K562 cells. We detected miR-27a expression after hemin stimulation at different time points. At the same time, the γ-globin gene also was measured via real-time PCR. According to the results of the chips, we screened the target protein of miR-27a through a dual-luciferase reporter assay and identified it via Western blot analyses. To evaluate the function of CDC25B, benzidine staining and flow cytometry were employed to detect the cell differentiation and cell cycle. Results: We found that miR-27a promotes hemin-induced erythroid differentiation of human K562 cells by targeting cell division cycle 25 B (CDC25B). Overexpression of miR-27a promotes the differentiation of hemin-induced K562 cells, as demonstrated by γ-globin overexpression. The inhibition of miR-27a expression suppresses erythroid differentiation, thus leading to a reduction in the γ-globin gene. CDC25B was identified as a new target of miR-27a during erythroid differentiation. Overexpression of miR-27a led to decreased CDC25B expression after hemin treatment, and CDC25B was up-regulated when miR-27a expression was inhibited. Moreover, the inhibition of CDC25B affected erythroid differentiation, as assessed by γ-globin expression. Conclusion: This study is the first report of the interaction between miR-27a and CDC25B, and it improves the understanding of miRNA functions during erythroid differentiation.

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Drug resistance-related microRNAs in hematological malignancies: Translating basic evidence into therapeutic strategies

Cited by 28 publications

References 171 publications

MicroRNA‐494 sensitizes colon cancer cells to fluorouracil through regulation of DPYD

MicroRNA‐494 sensitizes colon cancer cells to fluorouracil through regulation of DPYD

LncRNA FENDRR attenuates adriamycin resistance via suppressing MDR1 expression through sponging HuR and miR‐184 in chronic myelogenous leukaemia cells

MiR-27a Promotes Hemin-Induced Erythroid Differentiation of K562 Cells by Targeting CDC25B

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