TLR4 knockout protects mice from radiation-induced thymic lymphoma by downregulation of IL6 and miR-21

Liu, C; Gao, Fu; Li, B; Mitchel, R. E. J.; Liu, X; Lin, Jin‐Sying; Zhao, Lan‐Juan; Cai, Jianming

doi:10.1038/leu.2011.113

Cited by 39 publications

(43 citation statements)

References 6 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: 99%

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: 99%

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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“…For MTT assay, 500 cells per well were seeded in triplicate in a 96-well plate with complete growth medium. Cells were counted over 5 days using the MTT assay (Promega, Fitchburg, WI, USA) as described previously [22,23]. The data were measured by Microtiter plate reader 570-nm filters (Promega, USA ).…”

Section: Methodsmentioning

confidence: 99%

“…Detection is based on a click reaction [20], a copper catalyzed covalent reaction between an azide and an alkyne. Flow Cytometry Assay was performed by using CellQuest software (Becton Dickinson, Franklin Lakes, NJ, USA) as described previously [21,22]. For MTT assay, 500 cells per well were seeded in triplicate in a 96-well plate with complete growth medium.…”

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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“…Cells were counted over 5 days using the MTT assay (Promega, Fitchburg, WI, USA) as described previously [16,17,18]. The data were measured by Microtiter plate reader 570-nm filters (Promega, USA).…”

Section: Methodsmentioning

confidence: 99%

Down-Regulation of miR-3928 Promoted Osteosarcoma Growth

Liu

Zhao

2014

Cell Physiol Biochem

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Background: Osteosarcoma is the most common primary bone malignancy in children and young adults. Most failures of osteosarcoma treatment were due to resistance to chemotherapy. Development of new therapy required elucidation underlying molecular mechanism. Many miRNAs have been proved to be involved in the pathogenesis of osteosarcoma. Methods: MiR-3928 expression level was assayed by qRT-PCR. MiRNA mimics or ASO were transfected for up-regulation or down-regulation of miR-3928 expression. Cell proliferation was assayed by formazan test. Apoptosis and cell cycle were assayed by FACS. MiR-3928 targeted genes were predicated by bioinformatics algorithm (TargetScanHuman). The correlation between targeted gene and miR-3928 was analyzed by Pearson's correlation coefficient analysis. Results: MiR-3928 was down-regulated in osteosarcoma tissues. Over-expression of miR-3928 inhibited tumor growth, induced cell apoptosis, increased the percent of cells in G1 phrase and decreased the percent of cells in S phrase. Down-regulation of miR-3928 promoted cell proliferation. ERBB3, IL-6R and CDK6 may be the targeted genes of miR-3928. Conclusions: Down-expression of miR-3928 in osteosarcoma promoted tumor growth by targeting ERBB3, IL-6R and CDK6. MiR-3928 may be a potential therapy target worth further investigation.

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TLR4 knockout protects mice from radiation-induced thymic lymphoma by downregulation of IL6 and miR-21

Cited by 39 publications

References 6 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

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

Down-Regulation of miR-3928 Promoted Osteosarcoma Growth

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