MicroRNA-7/NF-κB signaling regulatory feedback circuit regulates gastric carcinogenesis

Zhao, Xiaodi; Lu, Yuanyuan; Guo, Hao; Xie, Hui; He, Lijie; Shen, Gao-Fei; Zhou, Jinfeng; Li, Ting; Hu, Songhua; Zhou, Lin; Han, Yanan; Liang, Shuli; Wang, Xin; Wu, Kaichun; Shi, Yongquan; Nie, Yongzhan; Fan, Daiming

doi:10.1083/jcb.201501073

Cited by 78 publications

(57 citation statements)

References 50 publications

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“…MiRNAs negatively modulate gene expression at the post-transcriptional level by interacting with 3’-untranslated regions (3’-UTR) of their target gene mRNA, leading to mRNA degradation or translational repression of target gene [7, 8]. Accumulating evidence has demonstrated that miRNAs are closely associated with the regulation of cellular differentiation [9], cell proliferation [10], apoptosis, hematopoiesis [11], angiogenesis and carcinogenesis in various tumors [12]. In addition, miRNAs also function as an important regulator of autophagy, a lysosomal-mediated pathway that contributes to degradation of cell waste proteins and damaged organelles.…”

Section: Introductionmentioning

confidence: 99%

MiR-34a Promotes Apoptosis and Inhibits Autophagy by Targeting HMGB1 in Acute Myeloid Leukemia Cells

Liu

Ren

Chen

2017

Cell Physiol Biochem

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Background: MiR-34a is identified as a tumor suppressor gene and involved in acute myeloid leukemia (AML) development. However, the regulatory mechanism of miR-34a in AML is unclear. Methods: The expression of miR-34a and HMGB1 in HL-60, THP-1 and HS-5 cells were detected by qRT-PCR and western blot. Lipofectamine 2000 was used to transfect with miR-34a mimics, miR-34a inhibitor, si-HMGB1, pcDNA 3.1-HMGB1, and corresponding controls. The apoptosis and autophagy of transfected AML cells were assessed by flow cytometry and western blot, respectively. Bioinformatics software and dual luciferase reporter assay were applied to predict and verify the target of miR-34a. The effects of miR-34a mimics or si-HMGB1 on chemotherapy-induced autophagy were further explored in HL-60 cells treated with all-trans retinoic acid (ATRA) along with lysosomal protease inhibitors E64d and pepstatin A. Results: MiR-34a was lower expressed and HMGB1 mRNA and proteins were both higher expressed in HL-60 and THP-1 cells compared with that in HS-5 cells. Higher expression levels of MiR-34 and lower expression levels of HMGB1 both significantly promoted apoptosis and inhibited autophagy in HL-60 and THP-1 cells. Dual luciferase reporter system confirmed that HMGB1 was a potential target of miR-34a. Moreover, overexpression of HMGB1 dramatically reversed the promotion of apoptosis and inhibition of autophagy mediated by higher expression level of miR-34a. Higher expression level of miR-34a and lower expression level of HMGB1 both inhibited chemotherapy-induced autophagy by stimulating the LC3 conversion. Conclusion: MiR-34a promoted cell apoptosis and inhibited autophagy by targeting HMGB1. Therefore, miR-34a may be a potential promising molecular target for AML therapy.

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Section: Introductionmentioning

confidence: 99%

MiR-34a Promotes Apoptosis and Inhibits Autophagy by Targeting HMGB1 in Acute Myeloid Leukemia Cells

Liu

Ren

Chen

2017

Cell Physiol Biochem

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“…Furthermore, microRNAs and microRNA biogenesis expression is normalized to sham values day three following injury. Interestingly, miR-150 which had reduced expression day one following injury; has been shown to have an inverse relationships between their expression and levels of inflammatory mediators (32–34, 38, 39, 41, 42). These findings are in agreement with our in vitro study.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of microRNA biogenesis in the small intestine after ethanol and burn injury

Morris

Hammer

Cannon

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Ethanol exposure at the time of burn injury is a major contributor to post-burn pathogenesis. Many of the adverse effects associated with ethanol and burn injury are linked to an impaired intestinal barrier. The combined insult causes intestinal inflammation, resulting in tissue damage, altered tight junction expression, and increased intestinal permeability. microRNAs play a critical role in maintaining intestinal homeostasis including intestinal inflammation and barrier function. Specifically, miR-150 regulates inflammatory mediators which can contribute to gut barrier disruption. The present study examined whether ethanol and burn injury alters expression of microRNA processing enzymes (Drosha, Dicer, and Argonaute-2) and miR-150 in the small intestine. Male mice were gavaged with ethanol (~2.9g/kg) 4 hours prior to receiving a ~12.5% total body surface area full thickness burn. One or three days after injury, mice were euthanized and small intestinal epithelial cells (IECs) were isolated and analyzed for expression of microRNA biogenesis components and miR-150. Dicer mRNA and protein levels were not changed following the combined insult. Drosha and Argonaute-2 mRNA and protein levels were significantly reduced in IECs one day after injury; which accompanied reduced miR-150 expression. To further determine the role of miR-150 in intestinal inflammation, young adult mouse colonocytes were transfected with a miR-150 plasmid and stimulated with LPS (100ng/mL). miR-150 overexpression significantly reduced IL-6 and KC protein levels compared to vector control cells challenged with LPS. These results suggest that altered microRNA biogenesis and associated decrease in miR-150 likely contributes to increased intestinal inflammation following ethanol and burn injury.

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“…miR-7 targets and inhibits IKKε and RELA expression, and IKKε and RELA were found to suppress pri-miR-7 expression. Direct binding of RELA to both MIR7-1 and MIR7-2 promoter regions was confirmed [ 31 ]. Further, ubiquitin-specific peptidase 18 (Usp18) negatively regulates miR-7 expression.…”

Section: Microrna-7 Expression and Regulationmentioning

confidence: 99%

Clinical Potential of microRNA-7 in Cancer

Horsham

Kalinowski

Epis

et al. 2015

JCM

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microRNAs (miRNAs) are a family of short, non-coding RNA molecules that drive a complex network of post-transcriptional gene regulation by enhancing target mRNA decay and/or inhibiting protein synthesis from mRNA transcripts. They regulate genes involved in key aspects of normal cell growth, development and the maintenance of body homeostasis and have been closely linked to the development and progression of human disease, in particular cancer. Over recent years there has been much interest regarding their potential as biomarkers and as therapeutic agents or targets. microRNA-7 (miR-7) is a 23 nucleotide (nt) miRNA known primarily to act as a tumour suppressor. miR-7 directly inhibits a number of oncogenic targets and impedes various aspects of cancer progression in vitro and in vivo, however, some studies have also implicated miR-7 in oncogenic roles. This review summarises the role of miR-7 in cancer, its potential in miRNA-based replacement therapy and its capacity as both a diagnostic and prognostic biomarker.

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MicroRNA-7/NF-κB signaling regulatory feedback circuit regulates gastric carcinogenesis

Abstract: RELA and FOS are targets of miR-7 in gastric cancer cells and the miR-7/IKKε/RELA reciprocal feedback loop is important for gastric cancer induced by H. pylori infection.

Cited by 78 publications

References 50 publications

MiR-34a Promotes Apoptosis and Inhibits Autophagy by Targeting HMGB1 in Acute Myeloid Leukemia Cells

MiR-34a Promotes Apoptosis and Inhibits Autophagy by Targeting HMGB1 in Acute Myeloid Leukemia Cells

Dysregulation of microRNA biogenesis in the small intestine after ethanol and burn injury

Clinical Potential of microRNA-7 in Cancer

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