miR-9 regulates the multidrug resistance of chronic myelogenous leukemia by targeting ABCB1

Li, Yan; Zhao, Lifen; Li, Nana; Miao, Yuan; Zhou, Huimin; Li, Jia

doi:10.3892/or.2017.5464

Cited by 27 publications

(24 citation statements)

References 26 publications

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“…Since ERRα can regulate the mRNA stability of ABCB1, we then investigated whether miRNAs were involved in this process. The expression of miR‐9, miR‐200c, miR‐206, and miR‐495 was investigated in cells treated XCT‐790 due to they can directly bind to 3′UTR of ABCB1 to regulate its stability. Our data showed that XCT‐790 can increase the expression of miR‐9, while not others, in both MG‐63/Dox (Figure A) and HOS/Dox (Figure B) cells.…”

Section: Resultsmentioning

confidence: 99%

“…Various miRNAs such as miR‐9, miR‐200c, miR‐206, and miR‐495 can regulate the expression of ABCB1 in cancer cells. It has been confirmed by luciferase activity analysis that miR‐9 can direct bind to the 3′UTR of ABCB1 and then trigger its decay in cancer cells . As a transcription factor, ERRα might occupy the conserved ERRE in the promoter of miRNAs and then regulate their expression .…”

Section: Discussionmentioning

confidence: 99%

“…It has been confirmed by luciferase activity analysis that miR-9 can direct bind to the 3′UTR of ABCB1 and then trigger its decay in cancer cells. 26 As a transcription factor, ERRα might occupy the conserved ERRE in the promoter of miRNAs and then regulate their expression. 41 The mechanisms that XCT-790 induced up-regulation of miR-9 should be further investigated in the future.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Oestrogen‐related receptor alpha mediates chemotherapy resistance of osteosarcoma cells via regulation of ABCB1

Chen

Zhang

Yang

et al. 2019

J Cellular Molecular Medi

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Chemotherapy resistance is one of the major challenges for the treatment of osteosarcoma ( OS ). The potential roles of oestrogenic signals in the chemoresistance of OS cells were investigated. As compare to the parental cells, the doxorubicin and cisplatin ( CDDP ) resistant OS cells had greater levels of oestrogen‐related receptors alpha ( ERR α). Targeted inhibition of ERR α by its specific si RNA s or inverse agonist XCT ‐790 can restore the sensitivity of OS resistant cells to chemotherapy. This might be due to that si‐ ERR α can decrease the expression of P‐glycoprotein (P‐gp, encoded by ABCB 1), one important ABC membrane transporter for drug efflux. XCT ‐790 can decrease the transcription and mRNA stability of ABCB 1, while had no effect on protein stability of P‐gp. ERR α can bind to the transcription factor of SP 3 to increase the transcription of ABCB 1. Furthermore, XCT ‐790 treatment decreased the expression of miR‐9, which can bind to the 3′ UTR of ABCB 1 and trigger its decay. Collectively, we found that ERR α can regulate the chemoresistance of OS cells via regulating the transcription and mRNA stability of ABCB 1. Targeted inhibition of ERR α might be a potential approach for OS therapy.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Oestrogen‐related receptor alpha mediates chemotherapy resistance of osteosarcoma cells via regulation of ABCB1

Chen

Zhang

Yang

et al. 2019

J Cellular Molecular Medi

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“…Li et al . [82] , 2017 ABCC1 miR-1291 pancreatic cancer, lung cancer, kidney doxorubicin Pan et al . [88] , 2013…”

Section: K562 Cell Line Adriamycinmentioning

confidence: 99%

MicroRNAs and cancer drug resistance: over two thousand characters in search of a role

Gomes¹,

Rueff²,

Rodrigues³

2019

CDR

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MicroRNAs (miRNAs), a group of small regulatory noncoding RNAs, transformed our thinking on gene regulation. More than two thousand human miRNAs have been identified thus far. These bind imperfectly to the 3'-untranslated region of target mRNA and have been involved in several pathological conditions including cancer. In fact, major hallmarks of cancer, such as the cell cycle, cell proliferation, survival and invasion are modulated by miRNAs. Cancer drug resistance (CDR) has also been described as being modulated by miRNAs. CDR remains a burden for cancer therapy and patients' outcome, often resulting in more aggressive tumours that tend to metastasize to distant organs. In this review we discuss the role of miRNAs influencing drug metabolism and drug influx/efflux, two important mechanisms of CDR.

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“…MicroRNAs (miRNAs) are small non-coding RNA recently implicated in numerous biological processes through via regulating gene expression (5)(6)(7). Accumulating studies have reported the aberrant expression and key roles of several miRNAs in CML (8)(9)(10)(11)(12). Exploration of key miRNAs associated with CML development has become a hot topic of research.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of miR‑574‑3p suppresses proliferation and induces apoptosis of chronic myeloid leukemia cells via targeting IL6/JAK/STAT3 pathway

Yang

Zhang

et al. 2018

Exp Ther Med

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The present study aimed to elucidate the potential roles and regulatory mechanism of microRNA (miR)-574-3p in the development of chronic myeloid leukemia (CML). The expression of miR-574-3p in peripheral blood obtained from patients with CML was examined. Subsequently, miR-574-3p was overexpressed and suppressed in CML K562 cells to further investigate the effects of miR-574-3p on cell proliferation, and apoptosis. Furthermore, a luciferase reporter assay was performed to investigate whether interleukin-6 (IL-6) was a target of miR-574-3p. In addition, the regulatory association between miR-574-3p and the IL-6/Janus kinase (JNK)/signal transducer and activator of transcription-3 (STAT3) signaling pathway was explored. The expression of miR-574-3p in the peripheral blood obtained from patients with CML was significantly lower compared with that in healthy controls. Overexpression of miR-574-3p significantly inhibited the proliferation and induced the apoptosis of K562 cells, whereas suppression of miR-574-3p exhibited opposite effects. In addition, IL-6 was identified to be a direct target of miR-574-3p. Overexpression of IL-6 significantly promoted the proliferation and inhibited the apoptosis of K562 cells. Furthermore, overexpression of miR-574-3p inhibited the activation of the JAK/STAT3 signaling pathway, which was rescued by overexpression of IL-6. The results of the current study indicate that miR-574-3p overexpression may serve an important role in inhibiting proliferation and inducing apoptosis of K562 cells via suppression of IL-6/JAK/STAT3 signaling pathway activation. miR-574-3p may serve as a potential therapeutic target for CML.

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miR-9 regulates the multidrug resistance of chronic myelogenous leukemia by targeting ABCB1

Cited by 27 publications

References 26 publications

Oestrogen‐related receptor alpha mediates chemotherapy resistance of osteosarcoma cells via regulation of ABCB1

Oestrogen‐related receptor alpha mediates chemotherapy resistance of osteosarcoma cells via regulation of ABCB1

MicroRNAs and cancer drug resistance: over two thousand characters in search of a role

Overexpression of miR‑574‑3p suppresses proliferation and induces apoptosis of chronic myeloid leukemia cells via targeting IL6/JAK/STAT3 pathway

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