Emphasis on Adipocyte Transformation: Anti-Inflammatory Agents to Prevent the Development of Cancer-Associated Adipocytes

Of the various cell types in the tumor microenvironment (TME), adipocytes undergo a dynamic transformation when activated by neighboring cancer cells. Although these adipocytes, known as cancer-associated adipocytes (CAAs), have been reported to play a crucial role in tumor progression, the factors...

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Bibliographic Details
Published in:Cancers 2023-01, Vol.15 (2), p.502
Main Authors: Na, Heeju, Song, Yaechan, Lee, Han-Woong
Format: Article
Language:English
Subjects:
Adipocytes
Adipose tissue
Breast cancer
Cancer
Cyclooxygenase-2
Epidemiology
Genetic transformation
Inflammation
Lipids
Lipolysis
Metabolic disorders
Metabolites
Nonsteroidal anti-inflammatory drugs
Obesity
Phenotypes
Review
Tumor microenvironment
Tumors
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Summary:Of the various cell types in the tumor microenvironment (TME), adipocytes undergo a dynamic transformation when activated by neighboring cancer cells. Although these adipocytes, known as cancer-associated adipocytes (CAAs), have been reported to play a crucial role in tumor progression, the factors that mediate their transformation remain elusive. In this review, we discuss the hypothesis that inflammatory signals involving NF-ĸB activation can induce lipolysis and adipocyte dedifferentiation. This provides a mechanistic understanding of CAA formation and introduces the concept of preventing adipocyte transformation via anti-inflammatory agents. Indeed, epidemiological studies indicate a higher efficacy of nonsteroidal anti-inflammatory drugs (NSAIDs) in obese patients with cancer, suggesting that NSAIDs can modulate the TME. Inhibition of cyclooxygenase-2 (COX-2) and prostaglandin production leads to the suppression of inflammatory signals such as NF-ĸB. Thus, we suggest the use of NSAIDs in cancer patients with metabolic disorders to prevent the transformation of TME components. Moreover, throughout this review, we attempt to expand our knowledge of CAA transformation to improve the clinical feasibility of targeting CAAs.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers15020502