Abstract
The pre-metastatic niche is a favorable microenvironment for the colonization of metastatic tumor cells in specific distant organs. Lipid droplets (LDs, also known as lipid bodies or adiposomes) have increasingly been recognized as lipid-rich, functionally dynamic organelles within tumor cells, immune cells, and other stromal cells that are linked to diverse biological functions and human diseases. Moreover, in recent years, several studies have described the indispensable role of LDs in the development of pre-metastatic niches. This review discusses current evidence related to the biogenesis, composition, and functions of LDs related to the following characteristics of the pre-metastatic niche: immunosuppression, inflammation, angiogenesis/vascular permeability, lymphangiogenesis, organotropism, reprogramming. We also address the function of LDs in mediating pre-metastatic niche formation. The potential of LDs as markers and targets for novel antimetastatic therapies will be discussed.
Highlights
Metastasis is the primary cause of cancer morbidity and mortality[1]
Major advances in the understanding of LD regulation of cancer metastasis have been achieved in recent years
As an organelle that is centrally involved in cellular lipid balance and cellular signaling, our current understanding of LD dynamics, heterogeneity, and function in the PMN is still very limited
Summary
Metastasis is the primary cause of cancer morbidity and mortality[1]. Tumor metastasis is a complicated process termed the invasion-metastasis cascade, which involves multiple sequential and interrelated steps and several biochemical events. The metastatic cascade comprises the following sequential steps[2]: (1) tumor cells gain invasive activity and detach from the primary tumor site; (2) disseminated tumor cells (DTCs) break through the basement membrane (BM) and extracellular matrix (ECM) and invade the blood and/or lymphatic vessels; (3) circulating tumor cells (CTCs) escape immune elimination and survival in lymphatic and/or vascular circulation; (4) CTCs initiate extravasation, crossing from the vascular lumen into the organ parenchyma; and (5) CTCs survive and subsequently proliferate to form overt metastases in a secondary organ/site. A wealth of research has revealed that distant metastatic organs are not passive recipients of CTCs but instead selectively and actively prepare the secondary microenvironment in response to the primary tumor for CTC colonization before the arrival of CTCs8,9.
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