Bone Metastasis: Find Your Niche and Fit in

Zhang, Weijie; Bado, Igor; Wang, Hai; Lo, Hin-Ching; Zhang, Xiang H.-F.

doi:10.1016/j.trecan.2018.12.004

Cited by 77 publications

(47 citation statements)

References 193 publications

(223 reference statements)

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“…Meanwhile, premetastatic niches in the bone microenvironment are actively formed by secreted factors and/or exosomes from the primary tumor prior to DTC seeding (5,45,46). Upon arrival at the bone, DTCs that survive the hostile environment interact with the bone resident cells, forming the metastatic niche that determines the fate of DTCs (dormant, reactivated, or drug resistant) (5,7,9,47).…”

Section: Bone Metastasesmentioning

confidence: 99%

“…CTCs surviving in the circulation arrive at the bone marrow vasculatures and extravasate into bone marrow parenchyma. It is still unclear whether this process is completed by passive entry due to the discontinuous endothelium of bone marrow sinusoids or if any other pathway actively involved (6,7,93). Compared with other organs, the bone is unique for its mineral content, enriched vasculatures, low oxygen level, high local Ca 2+ concentration, and acidosis (94).…”

Section: Role Of the Upr On Colonization And Dormancymentioning

confidence: 99%

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Endoplasmic Reticulum Stress in Bone Metastases

Zhang

et al. 2020

Front. Oncol.

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Metastases-the spreading of cancer cells from primary tumors to distant organs, including bone-is often incurable and is the major cause of morbidity in cancer patients. Understanding how cancer cells acquire the ability to colonize to bone and become overt metastases is critical to identify new therapeutic targets and develop new therapies against bone metastases. Recent reports indicate that the endoplasmic reticulum (ER) stress and, as its consequence, the unfolded protein response (UPR) is activated during metastatic dissemination. However, their roles in this process remain largely unknown. In this review, we discuss the recent progress on evaluating the tumorigenic, immunoregulatory and metastatic effects of ER stress and the UPR on bone metastases. We explore new opportunities to translate this knowledge into potential therapeutic strategies for patients with bone metastases.

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Section: Bone Metastasesmentioning

confidence: 99%

Section: Role Of the Upr On Colonization And Dormancymentioning

confidence: 99%

Endoplasmic Reticulum Stress in Bone Metastases

Zhang

et al. 2020

Front. Oncol.

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“…Furthermore, cancer cell growth in bone marrow can be compromised by interferon (IFN)-mediated cytotoxic immune response by CD8 + T lymphocytes and natural killer cells [ 47 ]. These mechanisms together may result in frequently observed long-latency of bone metastasis [ 3 ] and their disruption may lead to the development of clinically evident bone metastasis.…”

Section: Bone Metastasis Processmentioning

confidence: 99%

“…At the final step of metastasis, the metastatic cancer cells should survive and grow at the metastatic organ by utilizing and adapting its microenvironment, which is totally different from that of their primary site. Similarly, in order to facilitate bone metastasis, cancer cells should exploit and modify the bone marrow microenvironment, which consists of a myriad of cell types including hematopoietic cells, endothelial cells, osteoclasts, osteoblasts, mesenchymal stromal cells (MSCs), and fibroblasts [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Emergence of Cancer-Associated Fibroblasts as an Indispensable Cellular Player in Bone Metastasis Process

Mukaida

Zhang

Sasaki

2020

Cancers

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Bone metastasis is frequently complicated in patients with advanced solid cancers such as breast, prostate and lung cancers, and impairs patients’ quality of life and prognosis. At the first step of bone metastasis, cancer cells adhere to the endothelium in bone marrow and survive in a dormant state by utilizing hematopoietic niches present therein. Once a dormant stage is disturbed, cancer cells grow through the interaction with various bone marrow resident cells, particularly osteoclasts and osteoblasts. Consequently, osteoclast activation is a hallmark of bone metastasis. As a consequence, the drugs targeting osteoclast activation are frequently used to treat bone metastasis but are not effective to inhibit cancer cell growth in bone marrow. Thus, additional types of resident cells are presumed to contribute to cancer cell growth in bone metastasis sites. Cancer-associated fibroblasts (CAFs) are fibroblasts that accumulate in cancer tissues and can have diverse roles in cancer progression and metastasis. Given the presence of CAFs in bone metastasis sites, CAFs are emerging as an important cellular player in bone metastasis. Hence, in this review, we will discuss the potential roles of CAFs in tumor progression, particularly bone metastasis.

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“…Bone marrow adipose tissue represents a distinct, heterogenous fat depot with an important role in hematopoiesis, skeletal biology, and tumors, known to provide a supportive microenvironment for hematological malignancies, such as multiple myeloma and leukemias, and a number of solid tumor metastases including melanoma (Chen et al, 2016) and breast and prostate tumors (Zhang et al, 2019). As BMAT expansion during aging interferes with hematopoietic stem/progenitor cell (HSPC) maintenance, BMAT appears as a negative regulator of hematopoiesis (Naveiras et al, 2009;Ambrosi et al, 2017).…”

Section: Bone Marrow Adipose Tissue and Neoplasmsmentioning

confidence: 99%

Adipogenesis in Different Body Depots and Tumor Development

Trivanović¹,

Petrinović

Djordjević

et al. 2020

Front. Cell Dev. Biol.

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Adipose tissue (AT) forms depots at different anatomical locations throughout the body, being in subcutaneous and visceral regions, as well as the bone marrow. These ATs differ in the adipocyte functional profile, their insulin sensitivity, adipokines' production, lipolysis, and response to pathologic conditions. Despite the recent advances in lineage tracing, which have demonstrated that individual adipose depots are composed of adipocytes derived from distinct progenitor populations, the cellular and molecular dissection of the adipose clonogenic stem cell niche is still a great challenge. Additional complexity in AT regulation is associated with tumor-induced changes that affect adipocyte phenotype. As an integrative unit of cell differentiation, AT microenvironment regulates various phenotype outcomes of differentiating adipogenic lineages, which consequently may contribute to the neoplastic phenotype manifestations. Particularly interesting is the capacity of AT to impose and support the aberrant potency of stem cells that accompanies tumor development. In this review, we summarize the current findings on the communication between adipocytes and their progenitors with tumor cells, pointing out to the coexistence of healthy and neoplastic stem cell niches developed during tumor evolution. We also discuss tumor-induced adaptations in mature adipocytes and the involvement of alternative differentiation programs.

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Bone Metastasis: Find Your Niche and Fit in

Cited by 77 publications

References 193 publications

Endoplasmic Reticulum Stress in Bone Metastases

Endoplasmic Reticulum Stress in Bone Metastases

Emergence of Cancer-Associated Fibroblasts as an Indispensable Cellular Player in Bone Metastasis Process

Adipogenesis in Different Body Depots and Tumor Development

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