Adipose Tumor Microenvironment

Zewdu, Abbie; Casadei, Lucia; Pollock, Raphael E.; Braggio, Danielle

doi:10.1007/978-3-030-36214-0_6

Cited by 9 publications

(4 citation statements)

References 147 publications

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“…Additionally, CCL2 and CCL5 can attract and modify the behavior of macrophages in AT, known as AT macrophages (ATMs), through the release of exosomes. ATMs have been associated with the production of various inflammatory substances [83], and their accumulation is frequently associated with adverse outcomes and resistance to cytotoxic therapy [84].…”

Section: Adipocytes In Ovarian Cancermentioning

confidence: 99%

Adipocyte Microenvironment in Ovarian Cancer: A Critical Contributor?

Duarte Mendes,

Freitas,

Vicente

et al. 2023

IJMS

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Ovarian cancer is one of the most common gynecological malignancies and has low survival rates. One of the main determinants of this unfavorable prognosis is the high rate of peritoneal metastasis at diagnosis, closely related to its morbidity and mortality. The mechanism underlying peritoneal carcinomatosis is not clearly defined, but a clear preference for omental spread has been described. Growing evidence suggests that adipose tissue plays a role in promoting cancer onset and progression. Moreover, obesity can lead to changes in the original functions of adipocytes, resulting in metabolic and inflammatory changes in the adipose tissue microenvironment, potentially increasing the risk of tumor growth. However, the specific roles of adipocytes in ovarian cancer have not yet been fully elucidated. Due to the undeniable link between obesity and cancer, the adipose tissue microenvironment could also present a promising therapeutic target that warrants further research. This review discusses the complex relationship between ovarian cancer and the adipose tissue microenvironment.

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Section: Adipocytes In Ovarian Cancermentioning

confidence: 99%

Adipocyte Microenvironment in Ovarian Cancer: A Critical Contributor?

Duarte Mendes,

Freitas,

Vicente

et al. 2023

IJMS

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“…e) CAAs are also an important source of adipokines, chemokines, cytokines and exosomes, which could facilitate tumor growth and regulate treatment responses [5][6][7]9]. CAAs secrete more chemokine (C-C motif) ligand 2 (CCL2), CCL5, interleukin-1β (IL-1β), IL-6, TNF-α, vascular endothelial growth factor (VEGF) and leptin, etc., which could facilitate the invasion of the tumor and immune escape [41]. For example, CCL2 and CCL5 can recruit macrophages and polarize them to M2-like subtype to form a specific structure called the crown-like structures (CLS).…”

Section: Caas As a Complex Assemblermentioning

confidence: 99%

Cancer-associated adipocytes as immunomodulators in cancer

et al. 2021

Biomark Res

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Cancer-associated adipocytes (CAAs), as a main component of the tumor-adipose microenvironment (TAME), have various functions, including remodeling the extracellular matrix and interacting with tumor cells or infiltrated leukocytes through a variety of mutual signals. Here, we summarize the primary interplay among CAAs, the immune response and cancer with a focus on the mechanistic aspects of these relationships. Finally, unifying our understanding of CAAs with the immune cell function may be an effective method to enhance the efficacy of immunotherapeutic and conventional treatments.

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“…The tumor microenvironment plays a pivotal role in orchestrating the malignant properties of TNBC cells [3,4]. Adipose tissue in the tumor microenvironment is attracting more attention because of its ability to secrete a lot of bioactive factors [5,6]. Adipose stem cells can produce leptin to enhance invasion and metastasis of TNBC cells [7].…”

Section: Introductionmentioning

confidence: 99%

Cancer-Associated Adipocytes Release FUCA2 to Promote Aggressive Phenotype in Triple-Negative Breast Cancer

Q¹,

Hui²,

Zhao³

et al. 2021

Preprint

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Background: Cancer-associated adipocytes (CAAs) have been suggested to promote tumor progression. Yet, the role of CAAs in triple-negative breast cancer (TNBC) is poorly investigated. Methods: We compared the expression of secretory protein-encoding genes in CAAs and control adipocytes. The effect of key secretory protein(s) on TNBC cell behaviors was explored. Results: CAAs expressed and secreted FUCA2 at greater levels than control adipocytes. When FUCA2 activity was blocked with a neutralizing antibody, TNBC cell proliferation and migration induced by CAA conditioned medium was impaired. In contrast, supplement of exogenous FUCA2 protein reinforced the proliferation, colony formation, and migration of TNBC cells. In vivo studies confirmed that FUCA2 exposure enhanced tumorigenesis and metastasis of TNBC cells. Mechanistic investigation revealed that FUCA2 induced TNBC aggressiveness through TM9SF3-dependent signaling. Depletion of TM9SF3 blocked CAA- and FUCA2-induced TNBC cell proliferation and migration. Compared to adjacent breast tissues, TNBC tissues had increased expression of TM9SF3. Moreover, high TM9SF3 expression was associated with advanced TNM stage, lymph node metastasis, and shorter overall survival of TNBC patients. Conclusions: Altogether, CAAs secrete FUCA2 to promote TNBC growth and metastasis through interaction with TM9SF3. Inhibition of TM9SF3 may represent a potential therapeutic strategy in the treatment of TNBC.

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Adipose Tumor Microenvironment

Cited by 9 publications

References 147 publications

Adipocyte Microenvironment in Ovarian Cancer: A Critical Contributor?

Adipocyte Microenvironment in Ovarian Cancer: A Critical Contributor?

Cancer-associated adipocytes as immunomodulators in cancer

Cancer-Associated Adipocytes Release FUCA2 to Promote Aggressive Phenotype in Triple-Negative Breast Cancer

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