Adipocytes in the Tumour Microenvironment

Pallegar, Nikitha K; Christian, Sherri L.

doi:10.1007/978-3-030-37184-5_1

Cited by 47 publications

(41 citation statements)

References 108 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In turn, tumor-educated normal cells support cancer cell growth, survival, migration and invasion, leading to metastasis [10]. Chemokines in distant organs also recruit tumor cells and facilitate their dissemination [11,12], while the paracrine activity of molecules released by adipocytes modifies antitumor immunity [13]. Moreover, tumor cells promote angiogenesis directly and indirectly by increasing the proangiogenic activity of TAMs [14].…”

Section: Introductionmentioning

confidence: 99%

The CCL5/CCR5 Axis in Cancer Progression

Aldinucci

Borghese

Casagrande

2020

Cancers

286

191

View full text Add to dashboard Cite

Tumor cells can “hijack” chemokine networks to support tumor progression. In this context, the C-C chemokine ligand 5/C-C chemokine receptor type 5 (CCL5/CCR5) axis is gaining increasing attention, since abnormal expression and activity of CCL5 and its receptor CCR5 have been found in hematological malignancies and solid tumors. Numerous preclinical in vitro and in vivo studies have shown a key role of the CCL5/CCR5 axis in cancer, and thus provided the rationale for clinical trials using the repurposed drug maraviroc, a CCR5 antagonist used to treat HIV/AIDS. This review summarizes current knowledge on the role of the CCL5/CCR5 axis in cancer. First, it describes the involvement of the CCL5/CCR5 axis in cancer progression, including autocrine and paracrine tumor growth, ECM (extracellular matrix) remodeling and migration, cancer stem cell expansion, DNA damage repair, metabolic reprogramming, and angiogenesis. Then, it focuses on individual hematological and solid tumors in which CCL5 and CCR5 have been studied preclinically. Finally, it discusses clinical trials of strategies to counteract the CCL5/CCR5 axis in different cancers using maraviroc or therapeutic monoclonal antibodies.

show abstract

Section: Introductionmentioning

confidence: 99%

The CCL5/CCR5 Axis in Cancer Progression

Aldinucci

Borghese

Casagrande

2020

Cancers

286

191

View full text Add to dashboard Cite

show abstract

“…These molecules are crucial for the physiology and development of AT and breast epithelium and for the entire organism. However, the same factors may as well contribute to proliferation, motility, invasiveness, epithelial to mesenchymal transition (EMT) and stemness of BC cells, as well as to tumor angiogenesis by activating different molecular mechanisms (12,(24)(25)(26) (19). However, lipids are taken up also by cancer cells which display a characteristic "lipid metabolic reprogramming."…”

Section: Mammary Adipose Tissue and Breast Cancermentioning

confidence: 99%

“…Leptin from obese-derived MSCs increases expression of SERPINE 1, SNAI2, IL-6, TWIST1, and cyclooxygenase-2 -COX-2, which are crucial in EMT and CSC programs in BC cell lines and in TNBC PDX-derived cells (72). Moreover, leptin modulates exosome biogenesis in BC cells and promotes invasive ductal and lobular carcinoma in vivo (12,73). Leptin increase and adiponectin reduction are hallmarks of obesity.…”

Section: Adipose Cells As Link Between Metabolic Derangements and Bc mentioning

confidence: 99%

“…Leptin increase and adiponectin reduction are hallmarks of obesity. While leptin involvement in BC progression is widely recognized (12,74), the role of adiponectin is still controversial and depends on ERα expression in BC (75). In ERα + cells, low adiponectin levels, like those observed in obesity, stimulate cell proliferation.…”

Section: Adipose Cells As Link Between Metabolic Derangements and Bc mentioning

confidence: 99%

“…Breast tissue is composed by 90% of adipose tissue (AT) with permanent interactions between epithelial cells and adipose cells (12). Adipocytes and their precursor mesenchymal stem cells (MSCs) may sustain tumor phenotypes by either acting as energy reservoirs for neighboring cancer cells or through secretion of signaling molecules and vesicles containing proteins, lipids and nucleic acids (13,14).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Mammary Adipose Tissue Control of Breast Cancer Progression: Impact of Obesity and Diabetes

et al. 2020

View full text Add to dashboard Cite

Mammary adipose tissue (AT) is necessary for breast epithelium. However, in breast cancer (BC), cell-cell interactions are deregulated as the tumor chronically modifies AT microenvironment. In turn, breast AT evolves to accommodate the tumor, and to participate to its dissemination. Among AT cells, adipocytes and their precursor mesenchymal stem cells (MSCs) play a major role in supporting tumor growth and dissemination. They provide energy supplies and release a plethora of factors involved in cancer aggressiveness. Here, we discuss the main molecular mechanisms underlining the interplay between adipose (adipocytes and MSCs) and BC cells. Following close interactions with BC cells, adipocytes lose lipids and change morphology and secretory patterns. MSCs also play a major role in cancer progression. While bone marrow MSCs are recruited by BC cells and participate in metastatic process, mammary AT-MSCs exert a local action by increasing the release of cytokines, growth factors and extracellular matrix components and become principal actors in cancer progression. Common systemic metabolic diseases, including obesity and diabetes, further modify the interplay between AT and BC. Indeed, metabolic perturbations are accompanied by well-known alterations of AT functions, which might contribute to worsen cancer phenotype. Here, we highlight how metabolic alterations locally affect mammary AT and interfere with the molecular mechanisms of bidirectional communication between adipose and cancer cells.

show abstract

The tumour microenvironment and metabolism in renal cell carcinoma targeted or immune therapy

Lai

Tang

Huang

et al. 2020

Journal Cellular Physiology

107

View full text Add to dashboard Cite

Renal cell carcinoma (RCC) is one of the most common tumours of the urinary system, and is insidious and not susceptible to chemoradiotherapy. As the most common subtype of RCC (70-80% of cases), clear cell renal cell carcinoma (ccRCC) is characterized by the loss of von Hippel-Lindau and the accumulation of robust lipid and glycogen. For advanced RCC, molecular-targeted drugs, tyrosine kinase inhibitors (TKIs) and the immune checkpoint inhibitors (ICIs) have been increasingly recommended and investigated. Due to the existence of a highly dynamic, adaptive and heterogeneous tumour microenvironment (TME), and due to the glucose and lipid metabolism in RCC, this cancer may be accompanied by various types of resistance to TKIs and ICIs. With the increased production of lactate, nitric oxide, and other new by-products of metabolism, novel findings of the TME and key metabolic enzymes drived by HIF and other factors have been increasingly clarified in RCC carcinogenesis and therapy. However, there are few summaries of the TME and tumour metabolism for RCC progression and therapy. Here, we summarize and discuss the relationship of the important implicated characteristics of the TME as well as metabolic molecules and RCC carcinogenesis to provide prospects for future treatment strategies to overcome TME-related resistance in RCC.

show abstract

Adipocytes in the Tumour Microenvironment

Cited by 47 publications

References 108 publications

The CCL5/CCR5 Axis in Cancer Progression

The CCL5/CCR5 Axis in Cancer Progression

Mammary Adipose Tissue Control of Breast Cancer Progression: Impact of Obesity and Diabetes

The tumour microenvironment and metabolism in renal cell carcinoma targeted or immune therapy

Contact Info

Product

Resources

About