MiR-487a resensitizes mitoxantrone (MX)-resistant breast cancer cells (MCF-7/MX) to MX by targeting breast cancer resistance protein (BCRP/ABCG2)

Ma, Mengtao; He, Miao; Wang, Yan; Jiao, Xuyang; Zhao, Lin; Bai, Xuefeng; Yu, Zhaojin; Wu, Huizhe; Sun, Mingli; Song, Zhiguo J.; Wei, Minjie

doi:10.1016/j.canlet.2013.07.016

Cited by 93 publications

(68 citation statements)

References 34 publications

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“…For instance, miR-451 and miR-326 are required for the chemosensitivity of breast cancer cells to doxorubicin via direct targeting of ABC family transporter genes ABCB1 and ABCC1 (MRP1), respectively [154,155]. Similarly, miR-487 a has been found to target ABCG2 to modulate the chemoresponsiveness of breast cancer cells to mitoxantrone [156]. Furthermore, it has been reported that miR-221/222 is responsible for tamoxifen resistance in luminal-type breast cancers by targeting p27Kip1, a cell-cycle inhibitor and tumor suppressor [109].…”

Section: The Roles Of Mirnas In Breast Cancer Stem Cells and Drug Resmentioning

confidence: 99%

Noncoding RNAs in breast cancer

Lo¹,

Wolfson²,

Zhou³

et al. 2015

Briefings in Functional Genomics

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The mammalian transcriptome has recently been revealed to encompass a large number of noncoding RNAs (ncRNAs) that play a variety of important regulatory roles in gene expression and other biological processes. MicroRNAs (miRNAs), the best studied of the short noncoding RNAs (sncRNAs), have been extensively characterized with regard to their biogenesis, function and importance in tumorigenesis. Another class of sncRNAs called piwi-interacting RNAs (piRNAs) has also gained attention recently in cancer research owing to their critical role in stem cell regulation. Long noncoding RNAs (lncRNAs) of >200 nucleotides in length have recently emerged as key regulators of developmental processes, including mammary gland development. lncRNA dysregulation has also been implicated in the development of various cancers, including breast cancer. In this review, we describe and discuss the roles of sncRNAs (including miRNAs and piRNAs) and lncRNAs in the initiation and progression of breast tumorigenesis, with a focus on outlining the molecular mechanisms of oncogenic and tumor-suppressor ncRNAs. Moreover, the current and potential future applications of ncRNAs to clinical breast cancer research are also discussed, with an emphasis on ncRNA-based diagnosis, prognosis and future therapeutics.

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Section: The Roles Of Mirnas In Breast Cancer Stem Cells and Drug Resmentioning

confidence: 99%

Noncoding RNAs in breast cancer

Lo¹,

Wolfson²,

Zhou³

et al. 2015

Briefings in Functional Genomics

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“…Cellular accumulation of doxorubicin was determined using the procedure originally notted by Ma MT et al, 26 with minor modifications. Briefly, MDR cells were seeded in 6-well plates.…”

Section: Doxorubicin Accumulation Assaymentioning

confidence: 99%

Dasatinib reverses the multidrug resistance of breast cancer MCF-7 cells to doxorubicin by downregulating P-gp expression via inhibiting the activation of ERK signaling pathway

Chen

Wang

Liu

et al. 2014

Cancer Biology & Therapy

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Keywords: dasatinib, doxorubicin, ERK pathway, multidrug resistance, P-glycoprotein Abbreviations: MDR, multidrug resistance; P-gp, P-glycoprotein; DOX, doxorubicin; ERKextracellular signal-regulated kinase; P-ERK, phosphorylated extracellular signal-regulated kinase.Multidrug resistance (MDR) is one of the major obstacles to the efficiency of cancer chemotherapy, which often results from the overexpression of drug efflux transporters such as P-glycoprotein (P-gp). In the present study, we determined the effect of dasatinib which was approved for imatinib resistant chronic myelogenous leukemia (CML) and (Ph C ) acute lymphoblastic leukemia (ALL) treatment on P-gp-mediated MDR. Our results showed that dasatinib significantly increased the sensitivity of P-gp-overexpressing MCF-7/Adr cells to doxorubicin in MTT assays; thus lead to an enhanced cytotoxicity of doxorubicin in MCF-7/Adr cells. Additionally, dasatinib increased the intracellular accumulation, inhibited the efflux of doxorubicin in MCF-7/Adr cells, and significantly enhanced doxorubicin-induced apoptosis in MCF-7/Adr cells. Further studies showed that dasatinib altered the expression levels of mRNA, protein levels of P-gp, and the phosphorylation of signal-regulated kinase (ERK) both in time-dependent (before 24 h) and dose-dependent manners at concentrations that produced MDR reversals. In conclusion, dasatinib reverses P-gpmediated MDR by downregulating P-gp expression, which may be partly attributed to the inhibition of ERK pathway. Dasatinib may play an important role in circumventing MDR when combined with other conventional antineoplastic drugs.

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“…There are several miRNA that have been identified in a wide range of cancer cells, as potential inhibitors of ABCG2 expression (such as miRNA-328, -hsa-miR-328, -519, -520h, -212, -181a, 487a and miR-302 [200][201][202][203][204][205] . The use of miRNA to interfere with transporter transcription confirmed the role of ABCG2 in drug resistance related signaling pathways.…”

Section: Abcg2 Inhibitorsmentioning

confidence: 99%

“…Use of microRNA has revealed a more complex role of ABCG2 in drug resistance related signaling pathways: SIRT1/CREB/ABCG2 and Wnt/β-catenin-ABCG2 pathway Breast, ovarian cancer, other cell lines [200][201][202][203][204][205][206][207] TKI: tyrosine kinase inhibitor; MDR: multidrug resistance; CML: chronic myeloid leukemia; NSCLC: non-small cell lung cancer their inhibition will also increase the oral bioavailability of the drug, in addition to its penetration to the tumor site. However, since these two transporters are also expressed in sanctuary sites, caution for potential toxic side effects should be considered.…”

Section: Dual Inhibitorsmentioning

confidence: 99%

How to overcome ATP-binding cassette drug efflux transporter-mediated drug resistance?

Jaramillo¹,

Saig²,

Cloos³

et al. 2018

CDR

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P-glycoprotein (ABCB1), multidrug resistance protein-1 (ABCC1) and breast cancer resistance protein (ABCG2) belong to the ATP-binding cassette (ABC) superfamily of proteins that play an important physiological role in protection of the body from toxic xenobiotics and endogenous metabolites. Beyond this, these transporters determine the toxicity profile of many drugs, and confer multidrug resistance (MDR) in cancer cells associated with a poor treatment outcome of cancer patients.It has long been hypothesized that inhibition of ABC drug efflux transporters will increase drug accumulation and thereby overcome MDR, but until now no approved inhibitor of these transporters is available in the clinic. In this review we present molecular strategies to overcome this type of drug resistance and discuss for each of these strategies their promising value or indicate underlying reasons for their limited success.

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MiR-487a resensitizes mitoxantrone (MX)-resistant breast cancer cells (MCF-7/MX) to MX by targeting breast cancer resistance protein (BCRP/ABCG2)

Cited by 93 publications

References 34 publications

Noncoding RNAs in breast cancer

Noncoding RNAs in breast cancer

Dasatinib reverses the multidrug resistance of breast cancer MCF-7 cells to doxorubicin by downregulating P-gp expression via inhibiting the activation of ERK signaling pathway

How to overcome ATP-binding cassette drug efflux transporter-mediated drug resistance?

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