Diabetes-associated dysregulated cytokines and cancer
- PMID: 29930868
- PMCID: PMC6007890
- DOI: 10.15761/ICST.1000173
Diabetes-associated dysregulated cytokines and cancer
Abstract
Epidemiological data demonstrate that patients with diabetes have an augmented risk of developing various types of cancers, accompanied by higher mortality. A number of mechanisms for this connection have been hypothesized, such as insulin resistance, hyperinsulinemia, hyperglycemia, and increased inflammatory processes. Apart from these potential mechanisms, several diabetes-associated dysregulated cytokines might be implicated in the link between diabetes and cancer. In fact, some inflammatory cytokines, e.g. TNF-α, IL-6 and leptin, have been revealed to play important roles in both initiation and progression of tumor. Here, we depict the role of these cytokines in key events of carcinogenesis and cancer development, including their capability to induce oxidative stress, inflammation, their participation in epithelial mesenchymal transition (EMT), angiogenesis, and metastasis. Finally, we will also highlight the existing knowledge in terms of the involvement of these cytokines in different cancer types and comment on potential significances for future clinical applications.
Keywords: angiogenesis; cancer; cytokine; diabetes mellitus; inflammation.
References
-
- Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ. Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data. Lancet. 2006;367:1747–1757. Crossref. - PubMed
-
- Cohen DH, LeRoith D. Obesity, type 2 diabetes, and cancer: the insulin and IGF connection. Endocr Relat Cancer. 2012;19:F27–45. Crossref. - PubMed
-
- Vigneri P, Frasca F, Sciacca L, Pandini G, Vigneri R. Diabetes and cancer. Endocr Relat Cancer. 2009;16:1103–1123. Crossref. - PubMed
-
- Jalving M, Gietema JA, Lefrandt JD, de Jong S, Reyners AK, et al. Metformin: taking away the candy for cancer? Eur J Cancer. 2010;46:2369–2380. Crossref. - PubMed
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