Mesenchymal Stromal Cells: Emerging Roles in Bone Metastasis

Graham, Nicola; Qian, Bin‐Zhi

doi:10.3390/ijms19041121

Cited by 35 publications

(30 citation statements)

References 277 publications

(401 reference statements)

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“…We subsequently reported that stromal cells from the primary tumor traveled to the metastasis site in a PDOX model of pancreatic cancer (20). Recently, our results that stromal cells are essential for cancer cell homing and colonization to other organs have been confirmed (28)(29)(30).…”

Section: Resultssupporting

confidence: 58%

“…All animal studies were conducted with an AntiCancer Institutional Animal Care and Use Committee (IACUC) protocol specifically approved for this study and in accordance with the principles and procedures outlined in the National Institute of Health Guide for the Care and Use of Animals under Assurance Number A3873-1. Mouse housing, feeding, surgical processes and imaging were conducted as previously described (23)(24)(25)(26)(27)(28)(29). The mice were humanely sacrificed as previously described (22)(23)(24)(25)(26).…”

Section: Methodsmentioning

confidence: 99%

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Detection of Metastasis in a Patient-derived Orthotopic Xenograft (PDOX) Model of Undifferentiated Pleomorphic Sarcoma with Red Fluorescent Protein

et al. 2018

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Section: Resultssupporting

confidence: 58%

Section: Methodsmentioning

confidence: 99%

Detection of Metastasis in a Patient-derived Orthotopic Xenograft (PDOX) Model of Undifferentiated Pleomorphic Sarcoma with Red Fluorescent Protein

et al. 2018

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“…During the past decade, strong evidence has been demonstrated MSCs-based therapy is a rapidly developing field for diseases due to their multiple modes of action that collectively respond to many of the fundamental pathologic events [ 22 , 23 ]. MSCs were originally identified in the bone marrow and later detected in many other tissues.…”

Section: Discussionmentioning

confidence: 99%

Autophagy induces G0/G1 arrest and apoptosis in menstrual blood-derived endometrial stem cells via GSK3-β/β-catenin pathway

Zhu

Guo

et al. 2018

Stem Cell Res Ther

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Background/aimsMenstrual blood-derived endometrial stem cells (MenSCs) emerge as an ideal source for cell-based treatment in regenerative medicine and immunotherapy. However, the major obstacle is the low survival rate in tissues and the limited expansion number. Autophagy is an intracellular metabolic self-degradative process which plays important roles in normal cellular division and survival, and the present study aimed to explore the related mechanisms between autophagy and survival of MenSCs in vitro and in vivo.MethodsThe MenSCs were obtained from menstrual blood procured from healthy female donors. In vitro, MenSCs were exposed to rapamycin and Earle’s balanced salts solution (EBSS). We evaluated the MenSCs immunophenotypic cell cycle distribution by propidium iodide (PI) staining and cell apoptosis by Annexin V/PI staining as well as their proliferative potential by the MTT assay. We also assessed the expression of genes associated with the cell cycle and Gsk3β signaling pathway by western blot analysis. We depressed Atg5 and Gsk3β expression by short hairpin RNA (shRNA) and undertook the experiments. Moreover, the labeled MenSCs were observed and counted with DiI after transplantation into the mice via the tail vein by microscopy in vivo.ResultsIn vitro, rapamycin and starvation induced autophagy of MenSCs. Hyperactive autophagy significantly induced G0/G1 arrest and slightly promoted apoptosis of MenSCs. Meanwhile, autophagy could stimulate p-GSK3β expression in MenSCs. Further, knockdown GSK3β can accelerate the proliferation of MenSCs by shRNA and CHIR99021. Moreover, the shGSK3β MenSCs showed strong proliferative activity in vitro and in vivo.ConclusionsOur results indicate that autophagy induced G0/G1 arrest and apoptosis of MenSCs via GSK3β/β-catenin pathway. Inhibiting autophagy or reduced GSK3β levels may improve survival rate in vivo, thus playing roles in MenSCs therapy.

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“…All of these factors are well-known to affect several hallmarks of cancer (60,61). Whereas, the contribution of CAFs to primary tumor growth is intensely investigated and defined, the origin and role of CAFs in the metastatic environment, especially in breast cancer bone metastasis, remain poorly defined (62). Within the next chapters we discuss evidence that supports a role of CAFs during the progression and establishment of breast cancer bone metastasis.…”

Section: Cancer Associated Fibroblasts In Breast Cancer (Bone) Metastmentioning

confidence: 98%

The Endosteal Niche in Breast Cancer Bone Metastasis

2020

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The establishment of bone metastasis remains one of the most frequent complications of patients suffering from advanced breast cancer. Patients with bone metastases experience high morbidity and mortality caused by excessive, tumor-induced and osteoclast-mediated bone resorption. Anti-resorptive treatments, such as bisphosphonates, are available to ease skeletal related events including pain, increased fracture risk, and hypercalcemia. However, the disease remains incurable and 5-year survival rates for these patients are below 25%. Within the bone, disseminated breast cancer cells localize in "metastatic niches," special microenvironments that are thought to regulate cancer cell colonization and dormancy as well as tumor progression and subsequent development into overt metastases. Precise location and composition of this "metastatic niche" remain poorly defined. However, it is thought to include an "endosteal niche" that is composed of key bone cells that are derived from both, hematopoietic stem cells (osteoclasts), and mesenchymal stromal cells (osteoblasts, fibroblasts, adipocytes). Our knowledge of how osteoclasts drive the late stage of the disease is well-established. In contrast, much less is known about the interaction between osteogenic cells and disseminated tumor cells prior to the initiation of the osteolytic phase. Recent studies suggest that mesenchymal-derived cells, including osteoblasts and fibroblasts, play a key role during the early stages of breast cancer bone metastasis such as tumor cell homing, bone marrow colonization, and tumor cell dormancy. Hence, elucidating the interactions between breast cancer cells and mesenchymal-derived cells that drive metastasis progression could provide novel therapeutic approaches and targets to treat breast cancer bone metastasis. In this review we discuss evidences reporting the interaction between tumor cells and endosteal niche cells during the early stages of breast cancer bone metastasis, with a particular focus on mesenchymal-derived osteoblasts and fibroblasts.

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Mesenchymal Stromal Cells: Emerging Roles in Bone Metastasis

Cited by 35 publications

References 277 publications

Detection of Metastasis in a Patient-derived Orthotopic Xenograft (PDOX) Model of Undifferentiated Pleomorphic Sarcoma with Red Fluorescent Protein

Detection of Metastasis in a Patient-derived Orthotopic Xenograft (PDOX) Model of Undifferentiated Pleomorphic Sarcoma with Red Fluorescent Protein

Autophagy induces G0/G1 arrest and apoptosis in menstrual blood-derived endometrial stem cells via GSK3-β/β-catenin pathway

The Endosteal Niche in Breast Cancer Bone Metastasis

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