A critical role of toll-like receptor 4 (TLR4) and its’ in vivo ligands in basal radio-resistance

Liu, C; Zhang, C; Mitchel, R. E. J.; Cui, Jianguo; Lin, Jin‐Sying; Yang, Yue; Liu, X; Cai, Jianming

doi:10.1038/cddis.2013.161

Cited by 54 publications

(71 citation statements)

References 30 publications

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“…Previously, it has been reported that doses in the range of 0.075-2 Gy increased the expression of TLR4-MD2 in mouse macrophages (12). Additionally, TLR4 was shown to be involved in the induction of radiation resistance (19), cell proliferation and the promotion of radiation-induced lymphomas (20), as well as the promotion of reactive oxygen and nitrogen species (ROS/RNS) causing the aggravation of chronic inflammatory diseases (21). One of the novel activators of TLR4 is HMGB1 (22).…”

Section: Discussionmentioning

confidence: 98%

Low doses of ionizing radiation induce immune-stimulatory responses in isolated human primary monocytes

El‐Saghire

Michaux

Thierens

et al. 2013

International Journal of Molecular Medicine

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Abstract. The health effects arising from exposure to low doses of ionizing radiation are of particular concern, mainly due to the increased application of diagnostic and therapeutic X-ray modalities. The mechanisms behind the cell and tissue responses to low doses remain to be elucidated. Accumulating evidence suggests that low doses of ionizing radiation induce activation of the immune response; however, the processes involved have yet to be adequately investigated. Monocytes are key players in the induction of an immune response. Within the context of this study, we investigated the activation of toll-like receptors (TLRs), mitogen-activated protein kinases (MAPKs) and NF-κB signaling in isolated human primary monocytes in response to low doses (0.05 and 0

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Section: Discussionmentioning

confidence: 98%

Low doses of ionizing radiation induce immune-stimulatory responses in isolated human primary monocytes

El‐Saghire

Michaux

Thierens

et al. 2013

International Journal of Molecular Medicine

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“…After different treatments, cells were marked with Annexin V-FITC and PI (propidium iodide) using an apoptosis detecting kit (Invitrogen, Canada) as described previously [37]. Samples were determined by FACS assays and the results were analyzed using CellQuest software (Becton Dickinson, San Jose, CA) [38].…”

Section: Methodsmentioning

confidence: 99%

Tumor-Suppressing Effect of MiR-4458 on Human Hepatocellular Carcinoma

Tang

Sun²,

Yu³

et al. 2015

Cell Physiol Biochem

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Background: Besides multiple genetic and epigenetic changes of protein coding genes in hepatocellular carcinoma (HCC), growing evidence indicate that deregulation of miRNAs contribute to HCC development by influencing cell growth, apoptosis, migration, or invasion. IKBKE is amplified and over-expressed in a large percentage of human breast tumors and identified as an oncogene of human breast tumor. Microarray analysis showed that miR-4458 was down-regulated in HCC tissues. Methods: The level of miR-4458 was up-regulated by miR-4458 mimics transfection, or down-regulated by miR-4458 ASO transfection. Cell proliferation was assayed by MTT analysis. MiRNAs and mRNA expression were assayed by qRT-PCR. These potential targeted genes of miR-4458 were predicted by bioinformatic algorithms. Dual luciferase reporter assay system was used to analyze the interaction between miR-4458 and IKBKE. IKBKE protein level was assayed by Western blot. The role of miR-4458 or IKBKE in the survival of HCC patients were revealed by Kaplan-Meier plot of overall survival. Results: Lower miR-4458 expression level or higher IKBKE level in HCC tissues correlated with worse prognosis of HCC patients. Overexpression of miR-4458 inhibited the HCC cells growth and vice versa. MiR-4458 played its role via targeting 3'UTR of IKBKE. Conclusions: MiR-4458 or IKBKE may be potential predictors of HCC prognosis. Restoration of miR-4458 or inhibition of IKBKE could be a prospective therapeutic approach for HCC.

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“…Cells were labeled with Annexin V-FITC and propidium iodide (PI) using an apoptosis detecting kit (Invitrogen, Canada) as described previously [31]. Samples were determined by FACS assays and the results were analyzed using CellQuest software (Becton Dickinson, San Jose, CA) [32].…”

Section: Methodsmentioning

confidence: 99%

miR-4782-3p Inhibited Non-Small Cell Lung Cancer growth via USP14

Zhang²,

Bai³

et al. 2014

Cell Physiol Biochem

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Background: Lung cancer is the leading cause of cancer-related mortality worldwide, with near 1.4 million deaths each year. NSCLC accounts for nearly 85% of all case of lung cancer. MiRNAs play important roles in regulation of gene expression at the post-transcriptional level. MiRNAs profiles may predict prognosis and disease recurrence in early-stage NSCLC. Our previous study proved that over-expression of ubiquitin specific peptidase 14 (USP14), a deubiquitinating enzyme, was associated with favorable prognosis in NSCLC patients and promoted tumor cells proliferation. Here, we tried to identify which miRNAs targeted USP14, and the roles of these miRNAs in NSCLC. Methods: MiR-4782-3p and its potential targeted genes were identified by bioinformatics algorithm. Dual luciferase reporter assay system was used to analyze the interaction between miR-4782-3p and targeted genes. Cell proliferation was assayed by MTT and BdU assay. MiRNAs and mRNA expression were assayed by qRT-PCR. USP14 protein level was assayed by Western blot. The role of miR-4782-3p in patients survival was revealed by Kaplan-Meier plot of overall survival. Results: Up-expression of miR-4782-3p in NSCLC cells decreased the USP14 expression. Down-expression of miR-4782-3p increased USP14 expression. In NSCLC specimen, Negative correlation between USP14 mRNA level and miR-4782-3p level was identified. Higher miR-4782-3p expression is associated with longer survival. USP14, ZEB2, XIAP overexpression reversed the inhibitory effect of miR-4782-3p. Conclusions: High expression of miR-4782-3p was associated with favorable prognosis in NSCLC patients. MiR-4782-3p inhibited cell proliferation in NSCLC by targeting USP14, ZEB2 and XIAP.

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A critical role of toll-like receptor 4 (TLR4) and its’ in vivo ligands in basal radio-resistance

Cited by 54 publications

References 30 publications

Low doses of ionizing radiation induce immune-stimulatory responses in isolated human primary monocytes

Low doses of ionizing radiation induce immune-stimulatory responses in isolated human primary monocytes

Tumor-Suppressing Effect of MiR-4458 on Human Hepatocellular Carcinoma

miR-4782-3p Inhibited Non-Small Cell Lung Cancer growth via USP14

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