Cited by 57Adipokines, Inflammation, and Metabolic DiseasesCytokine Signaling Pathways and InteractionsCancer Risks and Factors

An IL-6 link between obesity and cancer

Open access
Ghosh, Sagar·2013·Frontiers in Bioscience

Abstract

Obesity is a growing epidemic all over the world that by virtue of inducation of a chronic, low-grade, and systemic inflammation leads to an increased risk of a number of diseases, including cancer. IL-6 an important cytokine in the increased risk to cancer in obese patients mainly because of its pro-inflammatory activity. Some data suggest that IL-6 might increase the risk of certain cancers such as those that originate from breast, liver, prostate, colon, and esophagus. A better understanding of the regulation and role of IL-6 in obesity-associated cancer is required to develop effective therapeutic approaches.

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  • The enlargement of adipose tissue in obesity induces mechanical stress, ER stress and hypoxia in adipocytes, resulting in the release of free fatty acids and inflammatory cytokines such as IL-6 and TNFα and chemokines, suggesting activation of the IL-6 Amp.

    “The enlargement of adipose tissue in obesity induces mechanical stress, ER stress and hypoxia in adipocytes, resulting in the release of free fatty acids (FFAs) and inflammatory cytokines such as IL-6 and TNFα and chemokines (303–305), suggesting activation of the IL-6 Amp.”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [303]

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  • These events recruit macrophages, which further produce IL-6 and TNFα, major players involved in obesity-induced low-grade inflammation and cancer development.

    “Consistently, these events recruit macrophages, which further produce IL-6 and TNFα, major players involved in obesity-induced low-grade inflammation and cancer development (303, 304).”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [303]

    Section 4.1 (page unavailable) says adipose-tissue hypoxia can recruit macrophages and that obese adipose tissue secretes IL-6 and TNF-α, contributing to inflammation. Section 4.2 links these cytokines to cancer-related processes. The cited passages do not specifically establish that the recruited macrophages themselves produce both cytokines in this obesity-related sequence. (LLM, conf=0.82)

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  • Obesity causes chronic low-grade inflammation and is closely related with chronic inflammatory diseases, such as cardiovascular diseases and T2D, and some cancers, such as breast, liver and colon cancers.

    “Obesity causes chronic low-grade inflammation and is closely related with chronic inflammatory diseases, such as cardiovascular diseases and T2D and some cancers, such as breast, liver and colon cancers (233, 302–304).”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [303]

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References 187 · Cited by 57

Research works printed but not linked: 4

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Authors
Ghosh, S.
Affiliations
The University of Texas at San Antonio Health Science Center (US)
Corresponding author
Ghosh, Sagar
Venue
Frontiers in Bioscience
Publisher
IMR Press
Published
2013
Volume
E5
Issue
2
Pages
461-478
ISSN
  • 1944-7892 (ISSN-L)
  • 1945-0494
  • 1945-0508
OpenAlex
W1999208095
Cited by
57
References
187
Citations by year
2026: 1 · 2025: 5 · 2024: 2 · 2023: 7 · 2022: 5 · 2021: 3 · 2020: 2 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 6 · 2015: 3 · 2014: 8 · 2013: 5 · 2012: 2
FWCI
0.72
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Bioscience-Elite (publishedVersion)
  • PubMed (publishedVersion)
Funders
San Antonio Area Foundation
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Oncology › Cancer Risks and Factors
Keywords
interleukin-6, obesity, obesity-related cancer, low-grade inflammation, inflammatory cytokines, cancer risk, breast cancer, liver cancer, prostate cancer, colon cancer, esophageal cancer
MeSH terms
Gene Expression Regulation, Humans, Inflammation, Models, Biological, Neoplasms, Obesity, Neoplastic Stem Cells, Interleukin-6, Adipocytes

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