Adipose‑derived mesenchymal stem cells exhibit tumor tropism and promote tumorsphere formation of breast cancer cells

Chen, Yanqing; He, Yunfan; Wang, Xuecen; Lu, Feng; Gao, Jianhua

doi:10.3892/or.2019.7018

Cited by 28 publications

(30 citation statements)

References 67 publications

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“…Although adipose MSCs represent the most prominent cell type in the breast tumor microenvironment, very little attention was given to the adipose MSC population. Interestingly, growing research interest was noted in exploiting adipose MSCs in the cancer biology field due to their dual role as cancer promoters and suppressors [ 11 , 18 ]. Breast cancer cells are likely to disseminate during cancer progression and interact with MSCs in TME, releasing molecular signals contributing to the emergence of a subpopulation of cells that may go into a dormancy stage.…”

Section: Discussionmentioning

confidence: 99%

Adipose MSCs Suppress MCF7 and MDA-MB-231 Breast Cancer Metastasis and EMT Pathways Leading to Dormancy via Exosomal-miRNAs Following Co-Culture Interaction

Ali

Yeap

et al. 2020

Pharmaceuticals

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Globally, breast cancer is the most frequently diagnosed cancer in women, and it remains a substantial clinical challenge due to cancer relapse. The presence of a subpopulation of dormant breast cancer cells that survived chemotherapy and metastasized to distant organs may contribute to relapse. Tumor microenvironment (TME) plays a significant role as a niche in inducing cancer cells into dormancy as well as involves in the reversible epithelial-to-mesenchymal transition (EMT) into aggressive phenotype responsible for cancer-related mortality in patients. Mesenchymal stem cells (MSCs) are known to migrate to TME and interact with cancer cells via secretion of exosome- containing biomolecules, microRNA. Understanding of interaction between MSCs and cancer cells via exosomal miRNAs is important in determining the therapeutic role of MSC in treating breast cancer cells and relapse. In this study, exosomes were harvested from a medium of indirect co-culture of MCF7-luminal and MDA-MB-231-basal breast cancer cells (BCCs) subtypes with adipose MSCs. The interaction resulted in different exosomal miRNAs profiles that modulate essential signaling pathways and cell cycle arrest into dormancy via inhibition of metastasis and epithelial-to-mesenchymal transition (EMT). Overall, breast cancer cells displayed a change towards a more dormant-epithelial phenotype associated with lower rates of metastasis and higher chemoresistance. The study highlights the crucial roles of adipose MSCs in inducing dormancy and identifying miRNAs-dormancy related markers that could be used to identify the metastatic pattern, predict relapses in cancer patients and to be potential candidate targets for new targeted therapy.

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Section: Discussionmentioning

confidence: 99%

Adipose MSCs Suppress MCF7 and MDA-MB-231 Breast Cancer Metastasis and EMT Pathways Leading to Dormancy via Exosomal-miRNAs Following Co-Culture Interaction

Ali

Yeap

et al. 2020

Pharmaceuticals

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“…For instance, ADSCs secrete adipsin, an adipokine shown to enhance BCSC properties. In particular, adipsin is able to increase the sphere-forming capacity of BC cells and to drive tumor growth [ 139 , 140 ]. Likewise, ADSCs pretreated with the adipokine visfatin and subsequently cocultured with MDA-MB-231 cells enhanced their viability, migration, and tumorsphere formation capacity, as well as tumor growth and metastasis in preclinical models of BC [ 141 ].…”

Section: The Tumor Microenvironment and The Breast Cancer Stem Celmentioning

confidence: 99%

The Tumor Microenvironment as a Driving Force of Breast Cancer Stem Cell Plasticity

Fico

Santamaria-Martínez

2020

Cancers

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Tumor progression involves the co-evolution of transformed cells and the milieu in which they live and expand. Breast cancer stem cells (BCSCs) are a specialized subset of cells that sustain tumor growth and drive metastatic colonization. However, the cellular hierarchy in breast tumors is rather plastic, and the capacity to transition from one cell state to another depends not only on the intrinsic properties of transformed cells, but also on the interplay with their niches. It has become evident that the tumor microenvironment (TME) is a major player in regulating the BCSC phenotype and metastasis. The complexity of the TME is reflected in its number of players and in the interactions that they establish with each other. Multiple types of immune cells, stromal cells, and the extracellular matrix (ECM) form an intricate communication network with cancer cells, exert a highly selective pressure on the tumor, and provide supportive niches for BCSC expansion. A better understanding of the mechanisms regulating these interactions is crucial to develop strategies aimed at interfering with key BCSC niche factors, which may help reducing tumor heterogeneity and impair metastasis.

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“…Previous studies in the context of wound healing have reported profound NET formation and IL-8 secretion in plasma-treated human neutrophils, which could be detrimental for cancer treatment [142]. Other cells, such as the adipose mesenchymal stromal cells (AMSCs) possess proangiogenic, antiapoptotic, proliferative, and multipotent differentiation characteristics that are often associated with tumour initiation and metastasis [143]. AMSCs have immunosuppressive properties and a positive tropism towards the TME [144] where they can interfere with the maturation of DCs and the proliferation and differentiation of B cells and ECM composition [145].…”

Section: Cellular Components Of the Tumour Microenvironmentmentioning

confidence: 99%

Modifying the Tumour Microenvironment: Challenges and Future Perspectives for Anticancer Plasma Treatments

Privat-Maldonado

Bengtson

Razzokov

et al. 2019

Cancers

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Tumours are complex systems formed by cellular (malignant, immune, and endothelial cells, fibroblasts) and acellular components (extracellular matrix (ECM) constituents and secreted factors). A close interplay between these factors, collectively called the tumour microenvironment, is required to respond appropriately to external cues and to determine the treatment outcome. Cold plasma (here referred as ‘plasma’) is an emerging anticancer technology that generates a unique cocktail of reactive oxygen and nitrogen species to eliminate cancerous cells via multiple mechanisms of action. While plasma is currently regarded as a local therapy, it can also modulate the mechanisms of cell-to-cell and cell-to-ECM communication, which could facilitate the propagation of its effect in tissue and distant sites. However, it is still largely unknown how the physical interactions occurring between cells and/or the ECM in the tumour microenvironment affect the plasma therapy outcome. In this review, we discuss the effect of plasma on cell-to-cell and cell-to-ECM communication in the context of the tumour microenvironment and suggest new avenues of research to advance our knowledge in the field. Furthermore, we revise the relevant state-of-the-art in three-dimensional in vitro models that could be used to analyse cell-to-cell and cell-to-ECM communication and further strengthen our understanding of the effect of plasma in solid tumours.

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Adipose‑derived mesenchymal stem cells exhibit tumor tropism and promote tumorsphere formation of breast cancer cells

Cited by 28 publications

References 67 publications

Adipose MSCs Suppress MCF7 and MDA-MB-231 Breast Cancer Metastasis and EMT Pathways Leading to Dormancy via Exosomal-miRNAs Following Co-Culture Interaction

Adipose MSCs Suppress MCF7 and MDA-MB-231 Breast Cancer Metastasis and EMT Pathways Leading to Dormancy via Exosomal-miRNAs Following Co-Culture Interaction

The Tumor Microenvironment as a Driving Force of Breast Cancer Stem Cell Plasticity

Modifying the Tumour Microenvironment: Challenges and Future Perspectives for Anticancer Plasma Treatments

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