Abstract
Senescence is characterized by a permanent cell cycle arrest that is elicited in response to different stresses. In addition, senescent cells undergo multiple other phenotypic alterations, such as autophagy modulation, metabolic reprogramming, and the senescence-associated secretory phenotype (SASP). These senescence-related and inflammatory effects prevail within tumors and are strongly controlled by cancer properties, and inflammatory mediators further maintain and propagate the senescence process to adjacent cells. It is important to consider these detrimental effects that may drive tumorigenesis or cancer relapse. Importantly, cancer-associated adipocytes (CAAs) are one of the primary stromal cells in various tumor microenvironments and favor tumor progression by releasing various factors that can mediate local and systemic effects. However, it remains unclear whether CAAs possess senescent features. In this review, we discuss the complex relationship between senescence and CAAs and highlight important considerations for therapeutics.
Highlights
Adipocytes are one of the primary stromal cells present in multiple cancers, such as breast, ovarian and colorectal cancer (Nieman et al, 2011; Wu et al, 2019a)
The senescent characteristics of adipocytes and the mechanisms by which they affect the phenotype of tumor cells remain incompletely understood
The overlap in expression profiles between these two tumor-promoting cell types suggests that the regulatory pathways that are further characterized in senescent cells will be directly applicable in cancer-associated adipocytes (CAAs)
Summary
Adipocytes are one of the primary stromal cells present in multiple cancers, such as breast, ovarian and colorectal cancer (Nieman et al, 2011; Wu et al, 2019a). Cancer-associated adipocytes (CAAs) are considered to play an active role in the tumor microenvironment. Senescent cells within the microenvironment and their functionally analogous cousins, cancer-associated fibroblasts (CAFs), promote transformation by stimulating tumor growth, angiogenesis, and invasion (Ruhland et al, 2016; Milanovic et al, 2018).
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