Overexpression of CXCL3 can enhance the oncogenic potential of prostate cancer

Gui, Shi-Liang; Teng, Lichen; Wang, Shu-qiu; Liu, Shuang; Lin, Ying‐Li; Zhao, Xiao-Lian; Liu, Lei; Sui, Hongyu; Yang, Yang; Liang, Lichun; Wang, Molin; Li, Xinyi; Cao, Yu; Li, Fengying; Wang, Weiqun

doi:10.1007/s11255-016-1222-2

Cited by 55 publications

(56 citation statements)

References 25 publications

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“…Expression of CXCL1 is upregulated in more aggressive phenotype of BC and high expression of CXCL1 has been associated with reduced disease‐free survival . A recent report demonstrated that CXCL3 and its receptor CXCR2 were overexpressed in prostate cancer cells and expression levels of CXCL3 were closely related to metastatic prostate cancer . Moreover, CXCL3 is involved in the metastasis of breast cancer .…”

Section: Discussionmentioning

confidence: 96%

“…(30) A recent report demonstrated that CXCL3 and its receptor CXCR2 were overexpressed in prostate cancer cells and expression levels of CXCL3 were closely related to metastatic prostate cancer. (31) Moreover, CXCL3 is involved in the metastasis of breast cancer. (32) These findings suggested that CXCL1 and CXCL3 may be potential targets for cancer therapy, including BC.…”

Section: Discussionmentioning

confidence: 99%

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Dual tumor‐suppressors miR‐139‐5p and miR‐139‐3p targeting matrix metalloprotease 11 in bladder cancer

et al. 2016

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Our recent study of the microRNA (miRNA) expression signature of bladder cancer (BC) by deep‐sequencing revealed that two miRNA, microRNA‐139‐5p/microRNA‐139‐3p were significantly downregulated in BC tissues. The aim of this study was to investigate the functional roles of these miRNA and their modulation of cancer networks in BC cells. Functional assays of BC cells were performed using transfection of mature miRNA or small interfering RNA (siRNA). Genome‐wide gene expression analysis, in silico analysis and dual‐luciferase reporter assays were applied to identify miRNA targets. The associations between the expression of miRNA and its targets and overall survival were estimated by the Kaplan–Meier method. Gain‐of‐function studies showed that miR‐139‐5p and miR‐139‐3p significantly inhibited cell migration and invasion by BC cells. The matrix metalloprotease 11 gene (MMP11) was identified as a direct target of miR‐139‐5p and miR‐139‐3p. Kaplan–Meier survival curves showed that higher expression of MMP11 predicted shorter survival of BC patients (P = 0.029). Downregulated miR‐139‐5p or miR‐139‐3p enhanced BC cell migration and invasion in BC cells. MMP11 was directly regulated by these miRNA and might be a good prognostic marker for survival of BC patients.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Dual tumor‐suppressors miR‐139‐5p and miR‐139‐3p targeting matrix metalloprotease 11 in bladder cancer

et al. 2016

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“…Furthermore, it has also been demonstrated that CCL5 is up-regulated in the substantia nigra of PD mouse models and the neutralization of CCL5 protects against nigrostriatal degeneration (Chandra et al, 2016). CXCL3 has also been found to be upregulated other disease states (Martín-Fuentes et al, 2009; See et al, 2014; Gui et al, 2016). …”

Section: Discussionmentioning

confidence: 99%

Thymoquinone increases the expression of neuroprotective proteins while decreasing the expression of pro-inflammatory cytokines and the gene expression NFκB pathway signaling targets in LPS/IFNγ -activated BV-2 microglia cells

Cobourne-Duval

Taka

Mendonca

et al. 2018

Journal of Neuroimmunology

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Neuroinflammation and microglial activation are pathological markers of a number of central nervous system (CNS) diseases. Chronic activation of microglia induces the release of excessive amounts of reactive oxygen species (ROS) and pro-inflammatory cytokines. Additionally, chronic microglial activation has been implicated in several neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Thymoquinone (TQ) has been identified as one of the major active components of the natural product Nigella sativa seed oil. TQ has been shown to exhibit anti-inflammatory, anti-oxidative, and neuroprotective effects. In this study, lipopolysaccharide (LPS) and interferon gamma (IFNγ) activated BV-2 microglial cells were treated with TQ (12.5 μM for 24 h). We performed quantitative proteomic analysis using Orbitrap/Q-Exactive Proteomic LC-MS/ MS (Liquid chromatography-mass spectrometry) to globally assess changes in protein expression between the treatment groups. Furthermore, we evaluated the ability of TQ to suppress the inflammatory response using ELISArray™ for Inflammatory Cytokines. We also assessed TQ's effect on the gene expression of NFκB signaling targets by profiling 84 key genes via real-time reverse transcription (RT2) PCR array. Our results indicated that TQ treatment of LPS/IFNγ-activated microglial cells significantly increased the expression of 4 antioxidant, neuroprotective proteins: glutaredoxin-3 (21 fold; p < 0.001), biliverdin reductase A (15 fold; p < 0.0001), 3-mercaptopyruvate sulfurtransferase (11 fold; p < 0.01), and mitochondrial lon protease (> 8 fold; p < 0.001) compared to the untreated, activated cells. Furthermore, TQ treatment significantly (P < 0.0001) reduced the expression of inflammatory cytokines, IL-2 = 38%, IL-4 = 19%, IL-6 = 83%, IL-10 = 237%, and IL-17a = 29%, in the activated microglia compared to the untreated, activated which expression levels were significantly elevated compared to the control microglia: IL-2 = 127%, IL-4 = 151%, IL-6 = 670%, IL-10 = 133%, IL-17a = 127%. Upon assessing the gene expression of NFκB signaling targets, this study also demonstrated that TQ treatment of activated microglia resulted in > 7 fold down-regulation of several NFκB signaling targets genes, including interleukin 6 (IL6), complement factor B (CFB), chemokine (C–C motif) ligand 3 (CXCL3), chemokine (C–C) motif ligand 5 (CCL5) compared to the untreated, activated microglia. This modulation in gene expression counteracts the > 10-fold upregulation of these same genes observed in the activated microglia compared to the controls. Our results show that TQ treatment of LPS/IFNγ-activated BV-2 microglial cells induce a significant increase in expression of neuroprotective proteins, a significant decrease in expression inflammatory cytokines, and a decrease in the expression of signaling target genes of the NFκB pathway. Our findings are the first to show that TQ treatment increased the expression of these neuroprotective proteins (biliverdin reductase-A, 3-mercaptopyruvate sulfu...

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“…It has been reported that chemokines play an important role via influencing the inflammatory response in the tumorigenesis, growth and metastasis. For instance, Gui et al detected that CXCL3 was overexpressed and had a significant effect on migration of PCa cells . Singh et al proved that PC‐3 cells with higher CXCL16 showed higher migratory ability and invasive potential than LNCAP cells .…”

Section: Discussionmentioning

confidence: 99%

MiR‐206 inhibits proliferation and migration of prostate cancer cells by targeting CXCL11

Wang

Hui

et al. 2018

The Prostate

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Overexpression of CXCL3 can enhance the oncogenic potential of prostate cancer

Abstract: Our findings suggest that CXCL3 and its receptor CXCR2 are overexpressed in prostate cancer cells, prostate epithelial cells and prostate cancer tissues, which may play multiple roles in prostate cancer progression and metastasis.

Cited by 55 publications

References 25 publications

Dual tumor‐suppressors miR‐139‐5p and miR‐139‐3p targeting matrix metalloprotease 11 in bladder cancer

Dual tumor‐suppressors miR‐139‐5p and miR‐139‐3p targeting matrix metalloprotease 11 in bladder cancer

Thymoquinone increases the expression of neuroprotective proteins while decreasing the expression of pro-inflammatory cytokines and the gene expression NFκB pathway signaling targets in LPS/IFNγ -activated BV-2 microglia cells

MiR‐206 inhibits proliferation and migration of prostate cancer cells by targeting CXCL11

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