Abstract
Simple SummaryThis review discusses the important newly-established roles for bone marrow adipose tissue in cancer progression and highlights the research demonstrating great promise for clinically targeting the cells in oncology. Bone marrow adipose tissue expands during aging and in obesity. It primarily comprises bone marrow adipocytes (also known as fat cells) and can also contain other cells, such as pre-adipocytes, fibroblasts, macrophages, other immune cells, and endothelial cells. Bone marrow adipocytes are scattered throughout the hematopoietic or “red” marrow, or are densely packed in the marrow cavity, creating “yellow” marrow. Bone marrow biologists are interrogating many questions to understand the nature of bone marrow adipocytes, including how aging and obesity affect these cells; their origins, functions, and endocrine roles; and whether they can be targeted to treat osteoporosis. In parallel, and often in concert, cancer researchers are delineating the role of bone marrow adipocytes in oncology and their potential translational significance for future therapeutics.Cancers that grow in the bone marrow are for most patients scary, painful, and incurable. These cancers are especially hard to treat due to the supportive microenvironment provided by the bone marrow niche in which they reside. New therapies designed to target tumor cells have extended the life expectancy for these patients, but better therapies are needed and new ideas for how to target these cancers are crucial. This need has led researchers to interrogate whether bone marrow adipocytes (BMAds), which increase in number and size during aging and in obesity, contribute to cancer initiation or progression within the bone marrow. Across the globe, the consensus in the field is a unified “yes”. However, how to target these adipocytes or the factors they produce and how BMAds interact with different tumor cells are open research questions. Herein, we review this research field, with the goal of accelerating research in the network of laboratories working in this area and attracting bright scientists with new perspectives and ideas to the field in order to bring about better therapies for patients with bone cancers.
Highlights
Bone cancer is one of the most destructive and painful manifestations of malignancy, and is often terminal for patients with tumors that originate in other locations and disseminate through the bloodstream to the bone marrow
Bone cancers in general are reviewed throughout this Special Issue in depth, and this review will focus on the role of the bone marrow adipocyte (BMAd) in these malignancies
It is clear that BMAds can contribute to cancer through a variety of mechanisms, which fuels the quest in the field to understand and target BMAds or factors derived from these cells
Summary
Bone cancer is one of the most destructive and painful manifestations of malignancy, and is often terminal for patients with tumors that originate in other locations and disseminate through the bloodstream to the bone marrow. Their work demonstrated that despite this decreased marrow adiposity, trabecular bone loss associated with aging still occurred as normal, suggesting that bone loss during aging is not completely dependent on increased BMAT or changes in the pre-adipocyte or pre-osteoblast MSC [18]. They found that PPARγ expression in MSCs is important for cortical bone integrity and limiting cortical porosity during aging [18]. BMAds (bone marrow adipocytes); IL-6 (interleukin 6); IL-17 (interleukin 17); MCP1 (monocyte chemoattractant protein-1); SDF1 (stromal cell-derived factor 1); SCF (stem cell factor); IL-7 (interleukin 7); IL-15 (interleukin 15); IL-34 (interleukin 34); M-CSF (macrophage colony-stimulating factor); BMP-4 (Bone morphogenetic protein 4); CCL-19 (Chemokine ligand 19); CD36 (cluster of differentiation 36); FABP4 (fatty acid binding protein 4); FABP5 (fatty acid binding protein 5); CPT1 (Carnitine palmitoyltransferase I); HIF1a (hypoxia-inducible factor 1-alpha); ER (endoplasmic reticulum); JAK (janus kinase); STAT (signal transducer and activator of transcription protein); Atg (autophagy related 3); Atg (autophagy related 5); LC3 I-II (forms of the microtubule-associated proteins 1A/1B light chain 3B)
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