Identification and Functional Verification of MicroRNA-16 Family Targeting Intestinal Divalent Metal Transporter 1 (DMT1) in vitro and in vivo

Jiang, Shuxia; Guo, Songjun; Li, Huifang; Ni, Yingdong; Ma, Wenqiang; Zhao, Ruqian

doi:10.3389/fphys.2019.00819

Cited by 14 publications

(14 citation statements)

References 61 publications

(76 reference statements)

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“…miR-Let-7d binds to the 3′-UTR of DMT1-IRE decreasing its expression at both the mRNA and protein levels in K562 and HEL cells ( 81 ). miR-16 family members miR-16, miR-195, miR-497 and miR-15b have been shown to suppress intestinal DMT1 expression by targeting DMT1 3′-UTR in HCT116 cells ( 82 ). These miRNAs may be involved in ferroptosis by targeting DMT1.…”

Section: Role Of Ncrnas In Ferroptosis and Cancer Developmentmentioning

confidence: 99%

Regulation of ferroptosis by non‑coding RNAs in the development and treatment of cancer (Review)

Luo

Huang

et al. 2020

Oncol Rep

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Ferroptosis, a relatively recently discovered type of cell death that is iron dependent and nonapoptotic, is involved in the accumulation of lipid reactive oxygen species (ROS), and has been shown to serve a vital role in various pathological processes, including those underlying neurodegeneration, ischemic reperfusion injury, acute organ injury, and in particular, tumor biology. Emerging evidence has highlighted the roles of ferroptosis in the development and resistance to chemoradiotherapy in cancer. Recently, an increasing number of studies have shown that non-coding RNAs modulate the process of ferroptotic cell death, and this has further highlighted the potential of regulation of ferroptosis as a means of cancer management. Although these studies have highlighted the critical role of ferroptosis in cancer therapeutics, the roles of ferroptosis induced by non-coding RNAs in cancer development remain unclear. Herein, the current body of knowledge of ferroptosis in cancer is summarized and an overview of the mechanisms of ferroptosis and the functions of non-coding RNAs in regulating ferroptotic cell death are discussed. The future status of ferroptosis in cancer management is deliberated and strategies for treatment of therapy-resistant cancers are discussed.

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Section: Role Of Ncrnas In Ferroptosis and Cancer Developmentmentioning

confidence: 99%

Regulation of ferroptosis by non‑coding RNAs in the development and treatment of cancer (Review)

Luo

Huang

et al. 2020

Oncol Rep

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“…However, the regulatory miRNA of agrin has not been reported. In this study, we searched for putative miRNAs by using common prediction algorithms (miRDB, miRanda, and TargetScan) and selected three miRNAs with high scores in at least 2 algorithms simultaneously, as reported previously (Gong et al, 2015;Jiang et al, 2019). Subsequent studies indicated that only miR-144 could regulate the expression of agrin, and miR-144/agrin/MuSK axis might regulate NMJ formation in nerve sprouting and the development of original motor endplates.…”

Section: Discussionmentioning

confidence: 96%

Agrin Influences Botulinum Neurotoxin A-Induced Nerve Sprouting via miR-144-agrin-MuSK Signaling

Pan

Liu

et al. 2020

Front. Cell Dev. Biol.

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Botulinum neurotoxin (BoNT) has become a powerful therapeutic tool, and is extensively used in aesthetic medicine and in the treatment of neurological disorders. However, its duration of effect is limited, mainly owing to nerve sprouting. Inhibition of nerve sprouting to prolong the effective duration of BoNT is therefore of great clinical interest. However, appropriate interventional strategies to accomplish this are currently unavailable. In this study, we determined the role of the neurogenic regulator agrin in BoNT type A (BoNT/A)-induced nerve sprouting in a rat model. We then determined whether agrin could be used as an interventional target for prolonging the duration of effect of BoNT/A, and made a preliminary study of the upstream and downstream regulatory mechanisms by which agrin could influence the effective duration of BoNT/A. Our results showed that agrin was involved in the regulation of BoNT/A-induced nerve sprouting, and blocking of agrin function with anti-agrin antibody temporarily could delay muscle strength recovery and prolong the duration of BoNT/A effect. Moreover, agrin influenced the duration of BoNT/A effect by regulating downstream myogenic muscle-specific receptor tyrosine kinase (MuSK), and was simultaneously regulated by upstream miR-144. In conclusion, agrin could regulate BoNT/A-induced nerve sprouting through miR-144-agrin-MuSK signaling; it influences the effective duration of BoNT/A, and could find clinical application as an interventional target for prolonging the effect of BoNT/A.

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“…After 1 week of acclimatization, mice were divided into a negative control group (miR-SC, n = 15) and a miR-20b over-expression group (miR-20b, n = 15) and were subjected to the same diets. Plasmid transfection was performed with some modifications based on previous studies [30]. Briefly, 20 μg pcDNA3.1(+)-miRNAs plasmid (miR-SC or miR-20b) in 150 μL Opti-MEM medium (31985-070, Gibco, Carlsbad, California, USA) was mixed with 25 μL lipofectamine 2000 in 150 μL Opti-MEM medium, and the total mixture (300 μL) was incubated for 30 min at room temperature.…”

Section: Methodsmentioning

confidence: 99%

“…MiR-let-7d induces iron accumulation in endosomes by suppressing expression of an isoform of divalent metal transporter 1 (DMT1) of K562 cells [29]. In vitro and in vivo studies showed that the miRNA-16 family (miR-15b, miR-16, miR-195 and miR-497) inhibits the expression of intestinal DMT1 [30]. MiR-485-3p and miR-20a regulate intracellular iron homeostasis by directly targeting FPN, an iron exporting gene in lung cancer and HepG2 cells, respectively [31,32].…”

Section: Introductionmentioning

confidence: 99%

MiR-20b Down-Regulates Intestinal Ferroportin Expression In Vitro and In Vivo

Jiang

Fang

Liu

et al. 2019

Cells

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Ferroportin (FPN) is the only known cellular iron exporter in mammalian. However, post-transcriptional regulation of intestinal FPN has not yet been completely understood. In this study, bioinformatics algorithms (TargetScan, PicTar, PITA, and miRanda) were applied to predict, screen and obtain microRNA-17 family members (miR-17, miR-20a, miR-20b, and miR-106a) targeting FPN, ‘seed sequence’ and responding binding sites on the 3′untranslated region (3′UTR) region of FPN. Dual-luciferase reporter assays revealed miRNA-17 family members’ mimics decreased the luciferase activity, whereas their inhibitors increased the luciferase activity. Compared with the FPN 3′UTR wild type reporter, co-transfection of a miRNA-17 family members’ over-expression plasmids and FPN 3′UTR mutant reporters enhanced the luciferase activity in HCT116 cells. Transfection with miR-20b overexpression plasmid significantly enhanced its expression, and it inhibited endogenous FPN protein expression in Caco-2 cells. Additionally, tail-vein injection of miR-20b resulted in increasing duodenal miR-20b expression, decreasing duodenal FPN protein expression, which was closely related to lower plasma iron level in mice. Taken together, these data suggest that the miR-20b is identified to regulate intestinal FPN expression in vitro and in vivo, which will provide a potential target for intestinal iron exportation.

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Identification and Functional Verification of MicroRNA-16 Family Targeting Intestinal Divalent Metal Transporter 1 (DMT1) in vitro and in vivo

Cited by 14 publications

References 61 publications

Regulation of ferroptosis by non‑coding RNAs in the development and treatment of cancer (Review)

Regulation of ferroptosis by non‑coding RNAs in the development and treatment of cancer (Review)

Agrin Influences Botulinum Neurotoxin A-Induced Nerve Sprouting via miR-144-agrin-MuSK Signaling

MiR-20b Down-Regulates Intestinal Ferroportin Expression In Vitro and In Vivo

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