Abstract
The most serious aspect of neoplastic disease is the spread of cancer cells to secondary sites. Skeletal metastases can escape detection long after treatment of the primary tumour and follow-up. Bone tissue is a breeding ground for many types of cancer cells, especially those derived from the breast, prostate, and lung. Despite advances in diagnosis and therapeutic strategies, bone metastases still have a profound impact on quality of life and survival and are often responsible for the fatal outcome of the disease. Bone and the bone marrow environment contain a wide variety of cells. No longer considered a passive filler, bone marrow adipocytes have emerged as critical contributors to cancer progression. Released by adipocytes, adipokines are soluble factors with hormone-like functions and are currently believed to affect tumour development. Src-associated in mitosis of 68 kDa (Sam68), originally discovered as a protein physically associated with and phosphorylated by c-Src during mitosis, is now recognised as an important RNA-binding protein linked to tumour onset and progression of disease. Sam68 also regulates splicing events and recent evidence reports that dysregulation of these events is a key step in neoplastic transformation and tumour progression. The present review reports recent findings on adipokines and Sam68 and their role in breast cancer progression and metastasis.
Highlights
Bone metastases are a leading cause of death in patients with advanced breast and prostate cancers
The present review reports recent findings on adipokines and Src-associated in mitosis of 68 kDa (Sam68) and their role in breast cancer progression and metastasis
Once considered passive fillers of the bone marrow niche or cells that occupy the space after trabecular bone loss, adipocytes are known to be endocrine targets and to possess endocrine-like functions: besides responding to growth hormones, insulin, and thyroid hormone, they release a plethora of adipokines among which leptin and adiponectin [1]
Summary
Bone metastases are a leading cause of death in patients with advanced breast and prostate cancers. The present review focuses on these two factors and their possible roles in bone marrow colonization by breast carcinoma cells. A less known third type of adipose tissue is BMAT, which has garnered recent interest owing to its probable role in cancer progression. This discovery is relevant for breast and prostate carcinoma-derived metastasis and for multiple myeloma arising in the bone. Adipocytes exert a critical role in disease progression in the tumour microenvironment by providing cancer cells with fatty acids, pro-inflammatory cytokines, and proteases [13,14,15]. BMAT is crucial in the development of blood disease, in which BMAs directly interact with blood tumour cells in the bone marrow. BMAT has been identified as a key driver in the progression of multiple myeloma [1,18,19]
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