PTX3 gene activation in EGF-induced head and neck cancer cell metastasis

Chang, Wei Chiao; Wu, Shengyuan; Huang, Wan-Chen; Hsu, Jinn Yuan; Chan, Shih Hung; Wang, Ju Ming; Tsai, Jhih Peng; Chen, Ben Kuen

doi:10.18632/oncotarget.3482

Cited by 61 publications

(77 citation statements)

References 41 publications

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“…Consistent with this, studies show that a regulatory region within the human PTX3 promoter contains an NF-B-binding site (36) and that P. gingivalis GroEL can stimulate the transcriptional activity of NF-B (33). AKT activation is also involved in PTX3 expression, as determined by pretreatment of cells with the chemical inhibitor LY294002 (data not shown), an observation consistent with a previous report demonstrating that PI3K/AKT is essential for PTX3 activation (37). According to a previous report that IL-1 signaling phosphorylates AKT, followed by activation of downstream NF-B signaling (37), GroEL could activate the AKT signaling cascade, which subsequently activates the NF-B pathway.…”

Section: Figsupporting

confidence: 89%

Pseudomonas aeruginosa GroEL Stimulates Production of PTX3 by Activating the NF-κB Pathway and Simultaneously Downregulating MicroRNA-9

et al. 2017

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As one of the first lines of host defense, monocytes play important roles in clearing infected microbes. The defensive response is triggered by recognition of diverse microbial moieties, including released factors, which modulate host immune responses to establish a harsh environment for clinically important bacterial pathogens. In this study, we found that the expression of PTX3, a soluble form of pattern recognition receptor, was induced by infection with live Pseudomonas aeruginosa or treatment of cells with its supernatant. P. aeruginosa GroEL, a homolog of heat shock protein 60, was identified as one of the factors responsible for inducing the expression of PTX3 in host cells. GroEL induced PTX3 expression by activating the Toll-like receptor 4 (TLR4)-dependent pathway via nuclear factor-kappa B (NF-B), while simultaneously inhibiting expression of microRNA-9, which targets the PTX3 transcript. Finally, by acting as an opsonin, GroEL-induced PTX3 promoted the association and phagocytosis of Staphylococcus aureus into macrophages. These data suggest that the host defensive environment is supported by the production of PTX3 in response to GroEL, which thus has therapeutic potential for clearance of bacterial infections.

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Section: Figsupporting

confidence: 89%

Pseudomonas aeruginosa GroEL Stimulates Production of PTX3 by Activating the NF-κB Pathway and Simultaneously Downregulating MicroRNA-9

et al. 2017

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“…PTX3 promoter activity is strongly induced by these molecules through the activation of the NF-κB pathway [27, 49]. In this study, we further clarified that PTX3 was also induced in response to elevated oleate levels in cells.…”

Section: Discussionmentioning

confidence: 54%

“…The DNA fragment bearing the promoter region of PTX3 (1200 bp) was constructed as previously described [27]. …”

Section: Methodsmentioning

confidence: 99%

Oleate-induced PTX3 promotes head and neck squamous cell carcinoma metastasis through the up-regulation of vimentin

et al. 2017

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The association between metabolic diseases and the risk of developing cancer is emerging. However, the impact of long pentraxin-3 (PTX3) on dyslipidemia-associated tumor metastasis remains unknown. In this study, we found that oleate induced PTX3 expression and secretion through the activation of Akt/NF-κB pathway in head and neck squamous cell carcinomas (HNSCCs). The activation of NF-κB was essential for the oleate-induced stabilization of PTX3 mRNA. In addition, both the depletion of PTX3 and the inhibition of NF-κB significantly inhibited oleate-induced tumor cell migration and invasion. The enhancement of binding between tumor and endothelial cells was observed in oleate-treated cells but not in the depletion and neutralization of PTX3 with siPTX3 and anti-PTX3 antibodies, respectively. The levels of oleate-induced epithelial-mesenchymal transition (EMT) markers, such as vimentin and MMP-3, were significantly reduced in PTX3-depleted cells. Knocking down vimentin also repressed oleate-induced HNSCC invasion. Furthermore, the depletion of PTX3 blocked the oleate-primed metastatic seeding of tumor cells in the lungs. These results demonstrate that oleate enhances HNSCC metastasis through the PTX3/vimentin signaling axes. The inhibition of PTX3 could be a potential strategy for the treatment of dyslipidemia-mediated HNSCC metastasis.

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“…160 However, in head and neck tumors, PTX3 appears to promote tumor cell migration and invasion, while in gliomas tumor cell proliferation. 161,162 In gastric cancer, PTX3 expression is associated with the extent of tumor cell invasion, and PTX3 gene silencing results in a reduced cancer-related inflammation. 163 All together these results point to a flexible role of PTX3 in damaged tissue, that comprises interaction with various ligands, regulation of the activation of the complement system, of angiogenesis and of the organization of the ECM.…”

Section: Ptx3 In the Response To Tissue Damage And Repairmentioning

confidence: 99%

The long pentraxin PTX3: A prototypical sensor of tissue injury and a regulator of homeostasis

Erreni

Manfredi

Garlanda

et al. 2017

Immunological Reviews

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Tissue damage frequently occurs. The immune system senses it and enforces homeostatic responses that lead to regeneration and repair. The synthesis of acute phase molecules is emerging as a crucial event in this program. The prototypic long pentraxin PTX3 orchestrates the recruitment of leukocytes, stabilizes the provisional matrix in order to facilitate leukocyte and stem progenitor cells trafficking, promotes swift and safe clearance of dying cells and of autoantigens, limiting autoimmunity and protecting the vasculature. These non-redundant actions of PTX3 are necessary for the resolution of inflammation. Recent studies have highlighted the mechanisms by which PTX3 adapts the functions of innate immune cells, orchestrates tissue repair and contributes to select the appropriate acquired immune response in various tissues. Conversely, PTX3 continues to be produced in diseases where the inflammatory response does not resolve. It is therefore a valuable biomarker for more precise and personalized stratification of patients, often independently predicting clinical evolution and outcome. There is strong promise for novel therapies based on understanding the mechanisms with which PTX3 plays its homeostatic role, especially in regulating leukocyte migration and the resolution of inflammatory processes.

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PTX3 gene activation in EGF-induced head and neck cancer cell metastasis

Cited by 61 publications

References 41 publications

Pseudomonas aeruginosa GroEL Stimulates Production of PTX3 by Activating the NF-κB Pathway and Simultaneously Downregulating MicroRNA-9

Pseudomonas aeruginosa GroEL Stimulates Production of PTX3 by Activating the NF-κB Pathway and Simultaneously Downregulating MicroRNA-9

Oleate-induced PTX3 promotes head and neck squamous cell carcinoma metastasis through the up-regulation of vimentin

The long pentraxin PTX3: A prototypical sensor of tissue injury and a regulator of homeostasis

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