IL‐1α secreted by colon cancer cells enhances angiogenesis: The relationship between IL‐1α release and tumor cells' potential for liver metastasis

Matsuo, Yoichi; Sawai, Hirozumi; Ma, Jiachi; Xu, Donghui; Ochi, Nobuo; Yasuda, Akira; Takahashi, Hiroki; Funahashi, Hitoshi; Takeyama, Hiromitsu

doi:10.1002/jso.21245

Cited by 66 publications

(49 citation statements)

References 25 publications

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“…IL-1a, a key inflammatory cytokine, has been reported to be produced by various cancer cells derived from pancreas, lung, ovary and stomach, and to increase the invasive and metastatic capabilities of tumor cells [23,24]. Our data indicate that IL-1a secreted by SCC cells may enhance the CTSK expression of the surrounding Fbs in a paracrine fashion, which turns out to augment the invasive ability of SCC cells with support from CTSK-bearing Fbs.…”

Section: Discussionmentioning

confidence: 54%

Cathepsin K-upregulation in fibroblasts promotes matrigel invasive ability of squamous cell carcinoma cells via tumor-derived IL-1α

Xie¹,

Moroi²,

Hayashida³

et al. 2011

Journal of Dermatological Science

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Section: Discussionmentioning

confidence: 54%

Cathepsin K-upregulation in fibroblasts promotes matrigel invasive ability of squamous cell carcinoma cells via tumor-derived IL-1α

Xie¹,

Moroi²,

Hayashida³

et al. 2011

Journal of Dermatological Science

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“…A question that could be raised is why the conditioned media from cancer cell lines in this work did not have any pro-inflammatory cytokines, while other studies have shown that malignant cells do produce such interleukins. The possible answer could be that not all colon cancer cells produce cytokines as has been shown by Matsuo et al [24]. It is conceivable therefore, that aspirin affects colon carcinogenesis via several mechanisms.…”

Section: Discussionmentioning

confidence: 92%

Inflammation and Colorectal Cancer: Does Aspirin Affect the Interaction between Cancer and Immune Cells?

et al. 2010

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The effect of aspirin on colon-cancer-cell-induced cytokine secretion by peripheral blood mononuclear cells (PBMC) was examined. Aspirin was added to human colon cancer cells (HT-29 and RKO) or to PBMC incubated separately or jointly. The secretion of IFNγ, IL-6, and IL-10 induced by HT-29 cells was decreased, that of IL-1β was slightly increased, whereas IL-1ra production was not affected. With RKO cells, aspirin reduced IL-6, IL-1ra, and IL-10 synthesis and enhanced IFNγ secretion, while IL-1β remained unchanged. Conditioned media from colon cancer cells incubated without or with aspirin stimulated cytokine productions by PBMC similarly, suggesting that aspirin acts on the cell-to-cell interaction between cancer cells and PBMC. The results indicate that aspirin alter the balance between pro- and anti-inflammatory cytokines generated by interaction between colon cancer and immune cells disclosing an additional role of the drug in affecting inflammation-induced colon cancer.

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“…The process of EMT is induced, promoted and regulated by multiple effectors that also regulate EMT dur-ing embryogenesis, including the cytokines interleukin 8 (IL-8), growth factors [epidermal growth factor (EGF), platelet-derived growth factor (PDGF), TGFβ] and ECM components. Interestingly, it has been shown that CRC cells are able to produce such molecules, including IL-1α, IL-1β and tumour necrosis factor alpha (TNF-α) [60][61][62] . Specifically, TGFβ plays a critical role through autocrine and/or paracrine mechanisms.…”

Section: Transition Of Epithelial Cells In the Large Intestinementioning

confidence: 99%

Natural history of hepatic metastases from colorectal cancer - pathobiological pathways with clinical significance

Paschos

Majeed

Bird

2014

WJG

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Colorectal cancer hepatic metastases represent the final stage of a multi-step biological process. This process starts with a series of mutations in colonic epithelial cells, continues with their detachment from the large intestine, dissemination through the blood and/or lymphatic circulation, attachment to the hepatic sinusoids and interactions with the sinusoidal cells, such as sinusoidal endothelial cells, Kupffer cells, stellate cells and pit cells. The metastatic sequence terminates with colorectal cancer cell invasion, adaptation and colonisation of the hepatic parenchyma. All these events, termed the colorectal cancer invasion-metastasis cascade, include multiple molecular pathways, intercellular interactions and expression of a plethora of chemokines and growth factors, and adhesion molecules, such as the selectins, the integrins or the cadherins, as well as enzymes including matrix metalloproteinases. This review aims to present recent advances that provide insights into these cell-biological events and emphasizes those that may be amenable to therapeutic targeting. Paschos KA, Majeed AW, Bird NC. Natural history of hepatic metastases from colorectal cancer -pathobiological pathways with clinical significance.

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IL‐1α secreted by colon cancer cells enhances angiogenesis: The relationship between IL‐1α release and tumor cells' potential for liver metastasis

Abstract: Based on these findings, we conclude that colon cancer cell-derived IL-1alpha up-regulates angiogenesis by modulating stromal cells within the tumor cells' microenvironment.

Cited by 66 publications

References 25 publications

Cathepsin K-upregulation in fibroblasts promotes matrigel invasive ability of squamous cell carcinoma cells via tumor-derived IL-1α

Cathepsin K-upregulation in fibroblasts promotes matrigel invasive ability of squamous cell carcinoma cells via tumor-derived IL-1α

Inflammation and Colorectal Cancer: Does Aspirin Affect the Interaction between Cancer and Immune Cells?

Natural history of hepatic metastases from colorectal cancer - pathobiological pathways with clinical significance

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