Cancer cell-derived IL-1α induces IL-8 release in endothelial cells

Rhim, Jung Hyo; Kim, Sin Ae; Lee, Ji Eun; Kim, Dong Jo; Chung, Hyun Kee; Shin, Kum Joo; Chung, Junho

doi:10.1007/s00432-007-0243-8

Cited by 7 publications

(4 citation statements)

References 26 publications

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“…Targeting of IL‐1α or IL‐8 effectively inhibited phosphorylation of STAT3, decreased EMT and suppressed the invasiveness of breast cancer cells. In previous studies, IL‐1α and IL‐8 were found to be highly expressed in breast cancer compared with normal breast tissue, and associated with poor prognosis . Pantschenko et al .…”

Section: Discussionmentioning

confidence: 92%

“…In previous studies, IL-1a and IL-8 were found to be highly expressed in breast cancer compared with normal breast tissue, and associated with poor prognosis. (23)(24)(25)(26) Pantschenko et al (23) suggest that the IL-1 family of cytokines are present within human breast cancer and trigger other protumorigenic cytokines in tumor microenvironment, such as the angiogenic factor and growth factor including IL-8. In addition, they demonstrate that expression levels of some members of the IL-1 ⁄ IL-8 network of cytokines are correlated with prognostic indicators such as estrogen and progesterone receptors.…”

Section: Discussionmentioning

confidence: 99%

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Persistent activation of STAT3 by PIM2‐driven positive feedback loop for epithelial‐mesenchymal transition in breast cancer

et al. 2015

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Metastasis of breast cancer is promoted by epithelial–mesenchymal transition (EMT). Emerging evidence suggests that STAT3 is a critical signaling node in EMT and is constitutively activated in many carcinomas, including breast cancer. However, its signaling mechanisms underlying persistent activation of STAT3 associated with EMT remain obscure. Here, we report that PIM2 promotes activation of STAT3 through induction of cytokines. Activation of STAT3 caused an increase in PIM2 expression, implicating a positive feedback loop between PIM2 and STAT3. In agreement, targeting of either PIM2, STAT3 or PIM2-dependent cytokines suppressed EMT-associated migratory and invasive properties through inhibition of ZEB1. Taken together, our findings identify the signaling mechanisms underlying the persistent activation of STAT3 and the oncogenic role of PIM2 in EMT in breast cancer.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Persistent activation of STAT3 by PIM2‐driven positive feedback loop for epithelial‐mesenchymal transition in breast cancer

et al. 2015

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“…For these reasons, we wondered whether Gzm B-mediated processing of IL-1α could impact upon its biological activity. To explore this issue, we measured the ability of IL-1α to stimulate production of IL-6 and IL-8 from HeLa cells and primary HUVECs, as both cell types are known to respond to this cytokine (Bertelsen and Sanfridson, 2007; Rhim et al, 2008).…”

Section: Resultsmentioning

confidence: 99%

Granzyme B-Dependent Proteolysis Acts as a Switch to Enhance the Proinflammatory Activity of IL-1α

et al. 2011

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Granzyme B is a cytotoxic lymphocyte-derived protease that plays a central role in promoting apoptosis of virus-infected target cells, through direct proteolysis and activation of constituents of the cell death machinery. However, previous studies have also implicated granzymes A and B in the production of proinflammatory cytokines, via a mechanism that remains undefined. Here we show that IL-1α is a substrate for granzyme B and that proteolysis potently enhanced the biological activity of this cytokine in vitro as well as in vivo. Consistent with this, compared with full-length IL-1α, granzyme B-processed IL-1α exhibited more potent activity as an immunoadjuvant in vivo. Furthermore, proteolysis of IL-1α within the same region, by proteases such as calpain and elastase, was also found to enhance its biological potency. Thus, IL-1α processing by multiple immune-related proteases, including granzyme B, acts as a switch to enhance the proinflammatory properties of this cytokine.

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“…Using a HUVEC in vitro model, cancer cells were shown to secret interleukin (IL)-1α to stimulate IL-8 secretion by endothelial cells [41]. Moreover, conditioned medium of the A549 lung cancer cell line regulates endothelial cell platelet derived growth factor (PDGF) expression which is VEGF dependent [42].…”

Section: Discussionmentioning

confidence: 99%

Lysophosphatidic Acid Enhances Vascular Endothelial Growth Factor-C Expression in Human Prostate Cancer PC-3 Cells

et al. 2012

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Clinical evidence suggests that lymphangiogenesis and lymphatic metastasis are important processes during the progression of prostate cancer. Vascular endothelial growth factor (VEGF)-C was shown to be a key regulator in these processes. Our previous studies demonstrated that lysophosphatidic acid (LPA), a low-molecular-weight lipid growth factor, enhances VEGF-C expression in human endothelial cells. We previously demonstrated that the LPA receptor plays an important role in lymphatic development in zebrafish embryos. However, the effects of LPA on VEGF-C expression in prostate cancer are not known. Herein, we demonstrate that LPA up-regulated VEGF-C expression in three different human prostate cancer cell lines. In PC-3 human prostate cancer cells, the enhancing effects of LPA were mediated through both LPA1 and LPA3. In addition, reactive oxygen species (ROS) production and lens epithelium-derived growth factor (LEDGF) expression were involved in LPA1/3-dependent VEGF-C expression. Furthermore, autotaxin (ATX), an enzyme responsible for LPA synthesis, also participates in regulating VEGF-C expression. By interrupting LPA1/3 of PC-3, conditioned medium (CM) -induced human umbilical vein endothelial cell (HUVEC) lymphatic markers expression was also blocked. In summary, we found that LPA enhances VEGF-C expression through activating LPA1/3-, ROS-, and LEDGF-dependent pathways. These novel findings could potentially shed light on developing new strategies for preventing lymphatic metastasis of prostate cancer.

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Cancer cell-derived IL-1α induces IL-8 release in endothelial cells

Abstract: IL-1alpha is constitutively expressed in many human cancer cells and directly induces IL-8 secretion in neighboring endothelial cells.

Cited by 7 publications

References 26 publications

Persistent activation of STAT3 by PIM2‐driven positive feedback loop for epithelial‐mesenchymal transition in breast cancer

Persistent activation of STAT3 by PIM2‐driven positive feedback loop for epithelial‐mesenchymal transition in breast cancer

Granzyme B-Dependent Proteolysis Acts as a Switch to Enhance the Proinflammatory Activity of IL-1α

Lysophosphatidic Acid Enhances Vascular Endothelial Growth Factor-C Expression in Human Prostate Cancer PC-3 Cells

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