MyD88 as a target of microRNA-203 in regulation of lipopolysaccharide or Bacille Calmette-Guerin induced inflammatory response of macrophage RAW264.7 cells

Wei, Jun; Huang, Xuelan; Zhang, Zhaobo; Jia, Wei Hua; Zhi-gang, Zhao; Zhang, Ying; Liu, Xiaoming; Xu, Guofeng

doi:10.1016/j.molimm.2013.03.004

Cited by 69 publications

(36 citation statements)

References 38 publications

(40 reference statements)

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“…MiR-203 can be induced by LPS, IFN-b, and TNF-a in macrophages and keratinocytes [16,17]. Overexpression of miR-203 in RAW264.7 cells was correlated with repressions of MyD88, as well as its downstream signaling of NF-jB, TNF-a and IL-6 [18]. Moreover, inhibition of endogenous miR-203 elevated DKK1 expression, which may strengthen Wnt signaling and promote tumor initiation and metastasis in vivo [19].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-203 accelerates apoptosis in LPS-stimulated alveolar epithelial cells by targeting PIK3CA

Fang

et al. 2014

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 99%

MicroRNA-203 accelerates apoptosis in LPS-stimulated alveolar epithelial cells by targeting PIK3CA

Fang

et al. 2014

Biochemical and Biophysical Research Communications

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“…Therefore, there may be other molecules or signaling pathways that are also targeted by miR-203 (19,22,(47)(48)(49)(50), and some of them may be still unknown in NPC. This presumption may raise interesting future work to reveal the entire functions of miR-203 in NPC radioresistance.…”

Section: Discussionmentioning

confidence: 99%

MiRNA-203 Reduces Nasopharyngeal Carcinoma Radioresistance by Targeting IL8/AKT Signaling

et al. 2015

Molecular Cancer Therapeutics

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Radioresistance poses a major challenge in nasopharyngeal carcinoma (NPC) treatment, but little is known about how miRNA (miR) regulates this phenomenon. In this study, we investigated the function and mechanism of miR-203 in NPC radioresistance, one of downregulated miRs in the radioresistant NPC cells identified by our previous microarray analysis. We observed that miR-203 was frequently downregulated in the radioresistant NPC tissues compared with radiosensitive NPC tissues, and its decrement significantly correlated with NPC radioresistance and poor patient survival, and was an independent predictor for reduced patient survival. In vitro radioresponse assays showed that miR-203 mimic markedly decreased NPC cell radioresistance. In a mouse model, therapeutic administration of miR-203 agomir dramatically sensitized NPC xenografts to irradiation. Mechanistically, we confirmed that IL8 was a direct target of miR-203, and found that reduced miR-203 promoted NPC cell radioresistance by activating IL8/ AKT signaling. Moreover, the levels of IL8 and phospho-AKT were significantly increased in the radioresistant NPC tissues compared with radiosensitive NPC tissues, and negatively associated with miR-203 level. Our data demonstrate that miR-203 is a critical determinant of NPC radioresponse, and its decrement enhances NPC radioresistance through targeting IL8/AKT signaling, highlighting the therapeutic potential of the miR-203/IL8/AKT signaling axis in NPC radiosensitization. Mol Cancer Ther; 14(11); 2653-64. Ó2015 AACR.

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“…Among the “fine-tuners”, microRNAs are known to inhibit the expression of many key components of the TLR signaling program, including MyD88 (29, 30), IRAKs (31-33) and TRAF-6 (33-35). microRNAs can be produced constitutively or be upregulated by a variety of inflammatory stimuli, including LPS (21, 36-38), Poly(I:C) (37, 38) and TNF-α (36).…”

Section: Discussionmentioning

confidence: 99%

Leukotriene B4 Enhances the Generation of Proinflammatory MicroRNAs To Promote MyD88-Dependent Macrophage Activation

Wang

Filgueiras

Wang

et al. 2014

The Journal of Immunology

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MicroRNAs are known to control Toll like receptor activation in phagocytes. We have shown that leukotriene (LT) B4 (LTB4) positively regulates macrophage MyD88 expression by decreasing suppressor of cytokine signaling-1 (SOCS-1) mRNA stability. Here, we investigated the possibility that LTB4 control of MyD88 expression involves the generation of microRNAs. Our data show that LTB4, via its receptor B leukotriene receptor 1 (BLT1) and Gαi signaling, increased macrophage expression of inflammatory microRNAs, including miR-155, miR-146b, and miR-125b. LTB4-mediated miR-155 generation was attributable to AP-1 activation. Furthermore, macrophage transfection with antagomirs against miR-155 and miR-146b prevented both the LTB4-mediated decrease in SOCS-1 and increase in MyD88. Transfection with miR-155 and miR-146b mimics decreased SOCS-1 levels, increased MyD88 expression, and restored TLR4 responsiveness in both WT and LT-deficient macrophages. Together, our data unveil a heretofore unrecognized role for the GPCR BLT1 in controlling expression of microRNAs which regulate MyD88-dependent activation of macrophages.

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MyD88 as a target of microRNA-203 in regulation of lipopolysaccharide or Bacille Calmette-Guerin induced inflammatory response of macrophage RAW264.7 cells

Cited by 69 publications

References 38 publications

MicroRNA-203 accelerates apoptosis in LPS-stimulated alveolar epithelial cells by targeting PIK3CA

MicroRNA-203 accelerates apoptosis in LPS-stimulated alveolar epithelial cells by targeting PIK3CA

MiRNA-203 Reduces Nasopharyngeal Carcinoma Radioresistance by Targeting IL8/AKT Signaling

Leukotriene B4 Enhances the Generation of Proinflammatory MicroRNAs To Promote MyD88-Dependent Macrophage Activation

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