Systematic review of the association between circulating interleukin-6 (IL-6) and cancer

Heikkilä, Katriina; Ebrahim, Shah; Lawlor, Debbie A.

doi:10.1016/j.ejca.2008.02.047

Cited by 193 publications

(152 citation statements)

References 55 publications

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“…Inflammatory mediators, such as COX-2 and cytokines, enhance tumorigenesis through the activation of multiple signaling pathways in tumor tissue (17,37). IL6 is a major proinflammatory cytokine that participates in inflammation-associated carcinogenesis (38,39) and has been reported to be positively linked with angiogenesis, EMT, and poor prognosis in esophageal cancer (20). By cellular experiments, we found inhibition of IL6 decreased tumor growth and attenuated EMT similar to that induced by calcitriol.…”

Section: Discussionmentioning

confidence: 74%

1α,25-Dihydroxyvitamin D3 Inhibits Esophageal Squamous Cell Carcinoma Progression by Reducing IL6 Signaling

Chen

Hsieh

et al. 2015

Molecular Cancer Therapeutics

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The aim of this study was to highlight the role of 1a,25-dihydroxyvitamin D3 (calcitriol) in esophageal squamous cell carcinoma (SCC). The human esophageal SCC cell lines CE81T and TE2 were selected for cellular and animal experiments to investigate the changes in tumor behavior after calcitriol supplementation and the underlying mechanisms. Moreover, we evaluated the relationship between calcitriol supplementation, myeloid-derived suppressor cell (MDSC) recruitment, IL6 levels, and tumor progression by a 4-nitroquinoline 1-oxide (4-NQO)-induced esophageal tumor animal model. In this study, we demonstrated that calcitriol supplementation inhibited aggressive tumor behavior both in vitro and in vivo. The underlying changes included increased cell death, a lower degree of epithelial-mesenchymal transition, and inhibited IL6 signaling. In the 4-NQOinduced esophageal tumor animal model, increased IL6 and MDSC recruitment were linked with invasive esophageal tumors. Supplementation with calcitriol attenuated the level of IL6, the induction of MDSCs, and the incidence of 4-NQO-induced invasive tumors. Moreover, the IL6-induced changes in C57 mice, including augmented MDSC recruitment, increased levels of ROS and p-Stat3 in MDSCs, and higher suppressive function of MDSCs in T-cell proliferation, which were abrogated by calcitriol supplementation. On the basis of our results, we concluded that calcitriol abrogated the IL6-induced aggressive tumor behavior and MDSC recruitment to inhibit esophageal tumor promotion. Therefore, we suggest that supplementation with vitamin D 3 may be a promising strategy for the prevention and treatment of esophageal SCC.

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Section: Discussionmentioning

confidence: 74%

1α,25-Dihydroxyvitamin D3 Inhibits Esophageal Squamous Cell Carcinoma Progression by Reducing IL6 Signaling

Chen

Hsieh

et al. 2015

Molecular Cancer Therapeutics

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“…These data thus point out an important distinction between tumor formation in the oxa-colitis and DSS-colitis models: as shown in Supplemental Figure 7A, F4/80 + CD11b high Gr1 low cells were not present in the colons of mice with DSS-colitis with AOM-induced tumors, and, as shown in Supplemental Figure 7B, IL-13 levels in mice with DSS-colitis were quite low compared with those in mice with oxa-colitis on day 49.…”

Section: Nkt Cells Producing Il-13 Drive Chronic Oxa-colitis Previoumentioning

confidence: 97%

Tumor development in murine ulcerative colitis depends on MyD88 signaling of colonic F4/80+CD11bhighGr1low macrophages

Schiechl¹,

Bauer²,

Fuss³

et al. 2011

J. Clin. Invest.

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“…IL-6 protein and mRNA are also often upregulated in serum and tumor samples of humans and mice suffering from breast, prostate, lung, liver and colon cancer (Heikkila et al, 2008). IL-6 enhances the proliferation of human colon carcinoma cells in vitro and interference with IL-6 signaling during late stages of CAC development slows down tumor growth (Becker et al, 2004;Becker et al, 2005).…”

Section: Il-6 and Stat3mentioning

confidence: 99%

Signal Transducer and Activator of Transcription 3 - A Promising Target in Colitis-Associated Cancer

Pandurangan¹,

Esa²

2014

Asian Pacific Journal of Cancer Prevention

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Colorectal cancer (CRC) is the third most common malignancy and fourth most common cause of cancer mortality worldwide. Untreated chronic inflammation in the intestine ranks among the top three high-risk conditions for colitis-associated colorectal cancer (CAC). Signal Transducer and Activator of Transcription 3 (STAT3) protein is a member of the STAT family of transcription factors often deregulated in CRC. In this review, we try to emphasize the critical role of STAT3 in CAC as well as the crosstalk of STAT3 with inflammatory cytokines, nuclear factor (NF)-κB, PI3K/Akt, Mammalian Target of Rapamycin (mTOR), Notch, Wnt/β-catenin and microRNA (MiR) pathways. STAT3 is considered as a primary drug target to treat CAC in humans and rodents. Also we updated the findings for inhibitors of STAT3 with regard to effeects on tumorigenesis. This review will hopefully provide insights on the use of STAT3 as a therapeutic target in CAC.

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Systematic review of the association between circulating interleukin-6 (IL-6) and cancer

Cited by 193 publications

References 55 publications

1α,25-Dihydroxyvitamin D3 Inhibits Esophageal Squamous Cell Carcinoma Progression by Reducing IL6 Signaling

1α,25-Dihydroxyvitamin D3 Inhibits Esophageal Squamous Cell Carcinoma Progression by Reducing IL6 Signaling

Tumor development in murine ulcerative colitis depends on MyD88 signaling of colonic F4/80+CD11bhighGr1low macrophages

Signal Transducer and Activator of Transcription 3 - A Promising Target in Colitis-Associated Cancer

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