Suppression of IL‐8‐Src signalling axis by 17β‐estradiol inhibits human mesenchymal stem cells‐mediated gastric cancer invasion

Liu, Chung‐Jung; Kuo, Fu‐Chen; Wang, Chiu‐Lin; Kuo, Chao‐Hung; Wang, Sophie S.W.; Chen, Chiao‐Yun; Huang, Yaw‐Bin; Cheng, Kuang‐Hung; Yokoyama, Kazunari K.; Chen, Chunlin; Lu, Chien‐Yu; Wu, Deng‐Chyang

doi:10.1111/jcmm.12786

Cited by 19 publications

(16 citation statements)

References 38 publications

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“…A previous study found that seed cells contributed less to the final repair of bone tissue, compared to host-derived cells [12]. Here, we showed that BMSCs on tissue engineering bone release a large amount of IL-8, while some studies have shown that IL-8 is a chemotaxis to MSCs in vitro [33][34][35][36]. In this study, transwell experiments were done to confirm that IL-8 has a chemotactic effect on BMSCs.…”

Section: Discussionmentioning

confidence: 59%

IL-8 Enhances Therapeutic Effects of BMSCs on Bone Regeneration via CXCR2-Mediated PI3k/Akt Signaling Pathway

Yang

Xing

et al. 2018

Cell Physiol Biochem

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Background/Aims: Tissue engineering bone transplantation with bone marrow mesenchymal stem cells (BMSCs) is an effective technology to treat massive bone loss, while molecular regulation of the bone regeneration processes remains poorly understood. Here, we aimed to assess the role of interleukin-8 (IL-8) in the recruitment of host cells by seeded BMSCs and in the bone regeneration. Methods: A transwell assay was performed to examine the role of IL-8/CXCR1/CXCR2/PI3k/Akt on the migration potential of hBMSCs. The in vitro chondrogenic differentiation of hBMSCs was assessed by examination of 2 chondrogenic markers, Sox9 and type 2 collagen (COL2). mBMSCs were used in tissue engineered bone (TEB) with/without IL-8 implanted into bone defect area with CXCR2 or Akt inhibitors. Density and Masson staining of the regenerated bone were assessed. The chondrogenesis was assessed by expression levels of associated proteins, Sox9 and COL2, by RT-qPCR and by immunohistochemistry. Results: IL-8 may trigger in vitro migration of hBMSCs via CXCR2-mediated PI3k/Akt signaling pathway. IL-8 enhances osteogenesis in the TEB-implanted bone defect in mice. IL-8 induces chondrogenic differentiation of hBMSCs via CXCR2-mediated PI3k/Akt signaling pathway in vitro and in vivo. Conclusions: IL-8 enhances therapeutic effects of MSCs on bone regeneration via CXCR2-mediated PI3k/Akt signaling pathway.

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Section: Discussionmentioning

confidence: 59%

IL-8 Enhances Therapeutic Effects of BMSCs on Bone Regeneration via CXCR2-Mediated PI3k/Akt Signaling Pathway

Yang

Xing

et al. 2018

Cell Physiol Biochem

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“…Only a few studies have examined its anti-inflammatory effects on cells such as microglial cells (6,7) and macrophages (3). Furthermore, IL-8, a member of the CXC chemokine family, is involved in inflammatory responses, leukocyte chemotaxis and cancer development (18,19). The high expression of IL-8 is markedly associated with the proliferation, invasion and migration of gastric epithelial cells (20,21).…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of 1-tetradecanol on Helicobacter pylori-induced production of interleukin-8 and vascular endothelial growth factor in gastric epithelial cells

Kim

Kang

et al. 2017

Molecular Medicine Reports

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Helicobacter pylori (H. pylori) infection activates pro‑inflammatory mediators, including interleukin (IL)‑8 and vascular endothelial growth factor (VEGF) in gastric epithelial cells. 1‑Tetradecanol (1‑TD) has been purified from Dendropanax morbifera Leveille; its physiological activities are poorly understood. The present study assessed whether 1‑TD has an effect on H. pylori‑mediated inflammation in AGS gastric epithelial cells. 1‑TD reduced IL‑8 production by AGS cells in response to H. pylori in a significant and dose‑dependent manner, as measured by ELISA. Western blot analysis demonstrated that 1‑TD also suppressed the activation of nuclear factor‑κB, and two mitogen activated protein kinase species (p38 and extracellular signal‑regulated kinase 1/2), but not c‑Jun N‑terminal kinase in H. pylori‑infected AGS cells. As predicted, VEGF expression and hypoxia inducible factor‑1α stabilization induced by H. pylori in AGS cells were inhibited by 1‑TD. In addition, 1‑TD directly inhibited the growth of H. pylori in a dose‑dependent manner, as investigated by measuring the optical density. These findings indicated that 1‑TD may be a potential preventive or therapeutic agent for H. pylori‑induced gastric inflammation.

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“…Signals initiated by VEGF or IL-8 are transduced into cells through the activation of Src [29, 30]. A previous study shows that Src is an upstream of Vav2 in controlling Rac1 activation [43].…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that Src plays a critical role in regulating Rho GTPases such as Rac1, and one of the major functions of Src is to modulate the actin cytoskeleton that controls cell migration. A recent study reported that IL-8 up-regulated motility activity through Src signaling in human gastric cancer cells [29]. Src signaling has also been shown to be involved in VEGF-induced angiogenesis [30].…”

Section: Introductionmentioning

confidence: 99%

Autocrine VEGF and IL-8 Promote Migration via Src/Vav2/Rac1/PAK1 Signaling in Human Umbilical Vein Endothelial Cells

Li¹,

Zhou²,

Jiang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Pro-angiogenic factors VEGF and IL-8 play a major role in modulating the migratory potential of endothelial cells. The goal of this study was to investigate the effect of autocrine VEGF and IL-8 in the form of self-conditioned medium (CM) on human umbilical vein endothelial cells (HUVECs). Methods: Enzyme-linked immunosorbent assay (ELISA) examined the automatic secretion of VEGF and IL-8 protein by HUVECs. Western blot, small interfering RNA (siRNA), pulldown and Transwell assays were used to explore the role and the mechanism of autocrine VEGF and IL-8 in migration of HUVECs. Results: Neutralizing VEGF and IL-8 in CM significantly abrogated CM-induced migration of HUVECs. Autocrine VEGF and IL-8 increased Src phosphorylation, Rac1 activity and PAK1 phosphorylation in a time dependent manner. Additionally, blocking Rac1 activity with Rac1 siRNA largely abolished autocrine VEGF and IL-8-induced cell migration. Vav2 siRNA suppressed autocrine VEGF and IL-8-induced Rac1 activation and cell migration. Furthermore, blocking Src signaling with PP2, a specific inhibitor for Src, markedly prevented autocrine VEGF and IL-8-induced Vav2 and Rac1 activation as well as consequently cell migration. PAK1 siRNA also significantly abolished autocrine VEGF and IL-8-induced cell migration. Conclusions: We demonstrated for the first time that autocrine VEGF and IL-8 promoted endothelial cell migration via the Src/Vav2/Rac1/PAK1 signaling pathway. This finding reveals the molecular mechanism in the increase of endothelial cell migration induced by autocrine growth factors and cytokines, which is expected to provide a novel therapeutic target in vascular diseases.

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Suppression of IL‐8‐Src signalling axis by 17β‐estradiol inhibits human mesenchymal stem cells‐mediated gastric cancer invasion

Cited by 19 publications

References 38 publications

IL-8 Enhances Therapeutic Effects of BMSCs on Bone Regeneration via CXCR2-Mediated PI3k/Akt Signaling Pathway

IL-8 Enhances Therapeutic Effects of BMSCs on Bone Regeneration via CXCR2-Mediated PI3k/Akt Signaling Pathway

Inhibitory effect of 1-tetradecanol on Helicobacter pylori-induced production of interleukin-8 and vascular endothelial growth factor in gastric epithelial cells

Autocrine VEGF and IL-8 Promote Migration via Src/Vav2/Rac1/PAK1 Signaling in Human Umbilical Vein Endothelial Cells

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