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Obesity and Cancer Risk: Molecular Mechanisms and Perspectives

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 323

Special Issue Editor


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Guest Editor
Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire(UHCW), Coventry CV2 2DX, UK
Interests: obesity; diabetes; metabolism; energy homeostasis; neuroendocrinology

Special Issue Information

Dear Colleagues,

The global incidence and prevalence of obesity have dramatically risen over the last few decades. Epidemiological data suggest that obesity is associated with an increased risk of several, but not all, types of cancer, with marked gender-specific differences. The underlying mechanisms are still a matter of debate, with current experimental evidence suggesting the involvement of insulin resistance and low-grade inflammation in visceral fat tissue with the secretion of pro-inflammatory cytokines and adipokines, as well as an important role of sex hormones and gut microbiota. Most intriguingly, these factors contribute in a highly variable manner to the initiation of different tumor entities and eventually act directly or indirectly on the tumor environment to drive tumor progression. This also clearly implies that therapeutic strategies will have to be based on these mechanisms and must be precisely targeted. Understanding these mechanisms can be the basis for developing new, more effective therapeutic and preventive strategies and can improve the identification of obese people who are at very high risk of cancer.

This issue of IJMS is thus devoted to deciphering the molecular basis of tumor initiation and growth in obesity and providing a rational basis for precision management.

Prof. Dr. Hendrik Lehnert
Guest Editor

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Keywords

  • epidemiology of obesity and cancer
  • experimental models of cancer in obesity
  • genetic and epigenetics of obesity and metabolic dysfunction associated cancer
  • tumor microenvironment
  • basis of metastatic spread of cancer in obesity
  • therapeutic modeling and targeting

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Published Papers (1 paper)

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Review

17 pages, 1229 KiB  
Review
The Role of PAR2 in MASLD Progression and HCC Development
by Pietro Guerra, Patrizia Pontisso and Andrea Martini
Int. J. Mol. Sci. 2025, 26(15), 7076; https://doi.org/10.3390/ijms26157076 - 23 Jul 2025
Viewed by 64
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently become the leading cause of chronic liver disease and can progress to hepatocellular carcinoma (HCC) through multiple pathogenic mechanisms. Protease-activated receptor 2 (PAR2) is a G-protein-coupled receptor activated by proteases such as trypsin, tryptase or [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently become the leading cause of chronic liver disease and can progress to hepatocellular carcinoma (HCC) through multiple pathogenic mechanisms. Protease-activated receptor 2 (PAR2) is a G-protein-coupled receptor activated by proteases such as trypsin, tryptase or coagulation factors VII and Xa. Recent studies have shown that PAR2 expression is increased in the liver of patients with MASLD or liver fibrosis. Its activation is linked to metabolic dysfunction through several pathways, including SREBP1c activation, AMPK inhibition and Akt-induced insulin resistance. Inhibition of PAR2 has been effective in reducing MASLD progression in different animal models. Notably, PAR2 blockade has also been effective in more advanced stages of the disease by dampening chronic inflammation and fibrogenesis through the inhibition of hepatic stellate cell activation and of TGF-β and SerpinB3 production. PAR2 also plays a role in cancer development, promoting tumour proliferation, angiogenesis and expression of immune checkpoint inhibitors (like PD-L1, CD47 and CD24). Due to its multifaceted involvement in liver disease, PAR2 is emerging as a key therapeutic target in this clinical context. This review aims to summarise current knowledge on PAR2′s role in MASLD and its potential as a therapeutic target. Full article
(This article belongs to the Special Issue Obesity and Cancer Risk: Molecular Mechanisms and Perspectives)
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