Bradykinin stimulates IL-6 production and cell invasion in colorectal cancer cells

Wang, Guojun; Ye, Yanwei; Zhang, Xiefu; Song, Junmin

doi:10.3892/or.2014.3366

Cited by 35 publications

(31 citation statements)

References 32 publications

(33 reference statements)

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“…29,47,48 In the current study, we demonstrated that nicotine stimulated IL-6 production in endothelial EA.hy926 cells and, in turn, enhanced cell invasiveness. 29,47,48 In the current study, we demonstrated that nicotine stimulated IL-6 production in endothelial EA.hy926 cells and, in turn, enhanced cell invasiveness.…”

Section: Discussionsupporting

confidence: 59%

Nicotine stimulates IL‐6 expression by activating the AP‐1 and STAT‐3 pathways in human endothelial EA.hy926 cells

Ung

Nguyen

Lian

et al. 2018

J of Cellular Biochemistry

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Interleukin‐6 (IL‐6), a pleiotropic cytokine, plays a key role in endothelial injury and atherosclerosis. In this study, we investigated the effects of nicotine, a major psychoactive compound in cigarette smoke, on IL‐6 expression and EA.hy926 endothelial cell invasion. Nicotine stimulated IL‐6 expression via the activator protein 1 (AP‐1) transcription factor. Pharmacological inhibition and mutagenesis studies indicated that p38 mitogen‐activated protein kinase (MAPK) mediated the IL‐6‐induced upregulation of nicotine in EA.hy926 cells. Furthermore, the antioxidant compound N‐acetyl‐cysteine eliminated the nicotine‐activated production of reactive oxygen species (ROS) and inhibited signal transducer and activator of transcription 3 (STAT‐3) phosphorylation; these two mechanisms mediated the upregulation of IL‐6 expression by nicotine. In addition, the EA.hy926 cells treated with nicotine displayed markedly enhanced invasiveness due to IL‐6 upregulation. Our data demonstrate that nicotine induced IL‐6 expression, which, in turn, enhanced the invasiveness of endothelial EA.hy926 cells, via activation of the p38 MAPK/AP‐1 and ROS/STAT‐3 signaling pathways.

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Section: Discussionsupporting

confidence: 59%

Nicotine stimulates IL‐6 expression by activating the AP‐1 and STAT‐3 pathways in human endothelial EA.hy926 cells

Ung

Nguyen

Lian

et al. 2018

J of Cellular Biochemistry

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“…Previous studies showed the effects of bradykinin on stimulating cancer cells. For example, bradykinin can trigger proliferation, migration, and invasion of gastric cancer cells and cervical cancer cells via activation of the ERK and signal transducer and activator of transcription (STAT)-3 signaling pathways [35,36]. In hepatocellular carcinoma cells, bradykinin can trigger tumor metastasis [37].…”

Section: Discussionmentioning

confidence: 99%

The Bradykinin-BDKRB1 Axis Regulates Aquaporin 4 Gene Expression and Consequential Migration and Invasion of Malignant Glioblastoma Cells via a Ca2+-MEK1-ERK1/2-NF-κB Mechanism

Sun

Chen

Lin

et al. 2020

Cancers

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Glioblastoma multiforme (GBM) is the most common form of brain tumor and is very aggressive. Rapid migration and invasion of glioblastoma cells are two typical features driving malignance of GBM. Bradykinin functionally prompts calcium influx via activation of bradykinin receptor B1/B2 (BDKRB1/2). In this study, we evaluated the roles of bradykinin in migration and invasion of glioblastoma cells and the possible mechanisms. Expressions of aquaporin 4 (AQP4) mRNA and protein were upregulated in human glioblastomas. Furthermore, exposure of human U87 MG glioblastoma cells to bradykinin specifically increased levels of BDKRB1. Successively, bradykinin stimulated influx of calcium, phosphorylation of MEK1 and extracellular signal-regulated kinase (ERK)1/2, translocation and transactivation of nuclear factor-kappaB (NF-κB), and expressions of AQP4 mRNA and protein. Concomitantly, migration and invasion of human glioblastoma cells were elevated by bradykinin. Knocking-down BDKRB1 concurrently decreased AQP4 mRNA expression and cell migration and invasion. The bradykinin-induced effects were further confirmed in murine GL261 glioblastoma cells. Therefore, bradykinin can induce AQP4 expression and subsequent migration and invasion through BDKRB1-mediated calcium influx and subsequent activation of a MEK1-ERK1/2-NF-κB pathway. The bradykinin-BDKRB1 axis and AQP4 could be precise targets for treating GBM patients.

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“…The active peptide Bradykinin is released from HMW‐kininogen by Kallikrein cleavage and as mediator of inflammation shows a variety of physiological effects, such as: influence in smooth muscle contraction, induction of hypotension, and regulation of vascular permeability. It is known the role of Bradykinin in colon carcinogenesis (Graness et al, ; Wang et al, ). Controversially, we found the Bradykinin and des‐Arg 9 Bradykinin decreased in adenoma and CRC groups comparing to controls and this could be due to a different activation of peptidase‐mediated catabolic systems.…”

Section: Resultsmentioning

confidence: 99%

Alterations of the Plasma Peptidome Profiling in Colorectal Cancer Progression

Bedin

Crotti

Ragazzi

et al. 2015

Journal Cellular Physiology

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Early detection of colorectal cancer (CRC) remains a challenge. It has been highlighted that the pathological alterations within an organ and tissues might be reflected in serum or plasma proteomic/peptidic patterns. The aim of the study was to follow the changes in the plasma peptides associated to colorectal cancer progression by mass spectrometry. This study included 27 adenoma, 67 CRC (n = 33 I-II stage and n = 34 III-IV stage), 23 liver metastasis from CRC patients and 34 subjects disease-free as controls. For plasma peptides analysis, samples purification was performed on the Nanoporous Silica Chips technology followed by matrix-assisted laser desorption/ionisation-time of flight analysis. Since the high complexity of the obtained dataset, multivariate statistical analysis, and discriminant pattern recognition were performed for study groups classification. Forty-four of 88 ionic species were successfully identified as fragments of peptides and proteins physiologically circulating in the blood and belonging to immune and coagulation systems and inflammatory mediators. Many peptides clustered into sets of overlapping sequences with ladder-like truncation clearly associated to proteolytic processes of both endo- and exoproteases activity. Comparing to controls, a different median ion intensity of the group-type fragments distribution was observed. Moreover, the degradation pattern obtained by proteolytic cleavage was different into study groups. This pattern was specific and characteristic of each group: controls, colon tumour disease (including adenoma and CRC), and liver metastasis, revealing a role as biomarker in early diagnosis and prognosis. Our findings highlighted peculiar changes in protease activity characteristic of CRC progression from pre-cancer lesion to metastatic disease. J. Cell. Physiol. 231: 915-925, 2016. © 2015 Wiley Periodicals, Inc.

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Bradykinin stimulates IL-6 production and cell invasion in colorectal cancer cells

Cited by 35 publications

References 32 publications

Nicotine stimulates IL‐6 expression by activating the AP‐1 and STAT‐3 pathways in human endothelial EA.hy926 cells

Nicotine stimulates IL‐6 expression by activating the AP‐1 and STAT‐3 pathways in human endothelial EA.hy926 cells

The Bradykinin-BDKRB1 Axis Regulates Aquaporin 4 Gene Expression and Consequential Migration and Invasion of Malignant Glioblastoma Cells via a Ca2+-MEK1-ERK1/2-NF-κB Mechanism

Alterations of the Plasma Peptidome Profiling in Colorectal Cancer Progression

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