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Cellular Signalling in Cell Fusion
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Cellular Signalling in Cell Fusion

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 20129

Special Issue Editor

Prof. Dr. Thomas Dittmar

E-Mail Website
Guest Editor
Chair of Immunology, Witten/Herdecke University, 58448 Witten, Germany
Interests: cell fusion; breast cancer; stem cells; macrophages; inflammation; metastasis; drug resistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The biological phenomenon of cell fusion remains a mystery. Even though it is mandatory for several physiological and pathophysiological processes, considerably less is still known about it. Cell fusion is a tightly regulated process since cells are not fusogenic per se. They first have to be converted to a pro-fusogenic state in order to be able to hybridize. Subsequently, they have to assume a non-fusogenic state again.

But which signals and signal pathways are necessary for cells to assume a pro-fusogenic state and what does a pro-fusogenic state look like?

How do pro-fusogenic cells recognize their fusion partners and which proteins/mechanisms are involved? How is the cell fusion process ultimately terminated?

Which phenotype do hybrid cells adopt?

Do they remain at a multi-nuclear stage or does heterokaryon-to-synkaryon transition occur, which may be associated with aneuploidy?

These questions will be answered in this Special Issue.

Prof. Dr. Thomas Dittmar
Guest Editor

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Keywords

  • cell fusion
  • signal transduction
  • aneuploidy
  • cancer

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Published Papers (4 papers)

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Research

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20 pages, 1930 KiB  
Article
Spontaneous Fusion of MSC with Breast Cancer Cells Can Generate Tumor Dormancy
by Catharina Melzer, Juliane von der Ohe, Tianjiao Luo and Ralf Hass
Int. J. Mol. Sci. 2021, 22(11), 5930; https://doi.org/10.3390/ijms22115930 - 31 May 2021
Cited by 19 | Viewed by 3287
Abstract
Direct cellular interactions of MDA-MB-231cherry breast cancer cells with GFP-transduced human mesenchymal stroma/stem-like cells (MSCGFP) in a co-culture model resulted in spontaneous cell fusion by the generation of MDA-MSC-hyb5cherry GFP breast cancer hybrid cells. The proliferative capacity of MDA-MSC-hyb5 [...] Read more.
Direct cellular interactions of MDA-MB-231cherry breast cancer cells with GFP-transduced human mesenchymal stroma/stem-like cells (MSCGFP) in a co-culture model resulted in spontaneous cell fusion by the generation of MDA-MSC-hyb5cherry GFP breast cancer hybrid cells. The proliferative capacity of MDA-MSC-hyb5 cells was enhanced about 1.8-fold when compared to the parental MDA-MB-231cherry breast cancer cells. In contrast to a spontaneous MDA-MB-231cherry induced tumor development in vivo within 18.8 days, the MDA-MSC-hyb5 cells initially remained quiescent in a dormancy-like state. At distinct time points after injection, NODscid mice started to develop MDA-MSC-hyb5 cell-induced tumors up to about a half year later. Following tumor initiation, however, tumor growth and formation of metastases in various different organs occurred rapidly within about 10.5 days. Changes in gene expression levels were evaluated by RNA-microarray analysis and revealed certain increase in dormancy-associated transcripts in MDA-MSC-hyb5. Chemotherapeutic responsiveness of MDA-MSC-hyb5 cells was partially enhanced when compared to MDA-MB-231 cells. However, some resistance, e.g., for taxol was detectable in cancer hybrid cells. Moreover, drug response partially changed during the tumor development of MDA-MSC-hyb5 cells; this suggests the presence of unstable in vivo phenotypes of MDA-hyb5 cells with increased tumor heterogeneity. Full article
(This article belongs to the Special Issue Cellular Signalling in Cell Fusion)
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16 pages, 3227 KiB  
Article
Cell Fusion of Mesenchymal Stem/Stromal Cells and Breast Cancer Cells Leads to the Formation of Hybrid Cells Exhibiting Diverse and Individual (Stem Cell) Characteristics
by Jessica Dörnen, Ola Myklebost and Thomas Dittmar
Int. J. Mol. Sci. 2020, 21(24), 9636; https://doi.org/10.3390/ijms21249636 - 17 Dec 2020
Cited by 19 | Viewed by 3197
Abstract
Cancer is one of the most common diseases worldwide, and treatment bears many challenges such as drug and radioresistance and formation of metastases. These difficulties are due to tumor heterogeneity, which has many origins. One may be cell fusion, a process that is [...] Read more.
Cancer is one of the most common diseases worldwide, and treatment bears many challenges such as drug and radioresistance and formation of metastases. These difficulties are due to tumor heterogeneity, which has many origins. One may be cell fusion, a process that is relevant in both physiological (e.g., wound healing) and pathophysiological (cancer and viral infection) processes. In this study, we examined if cell fusion between mesenchymal stem/stromal cells (MSCs) and breast cancer (BC) cells occurs and if newly generated hybrid cells may exhibit cancer stem/initiating cell (CS/IC) characteristics. Therefore, several methods such as mammosphere assay, AldeRed assay, flow cytometry (CD24, CD44, CD104) and Western blot analysis (of epithelial to mesenchymal transition markers such as SNAIL, SLUG and Twist) were applied. In short, four different hybrid clones, verified by short tandem repeat (STR) analysis, were analyzed; each expressed an individual phenotype that seemed not to be explicitly related to either a more stem cell or cancer cell phenotype. These results show that cancer cells and MSCs are able to fuse spontaneously in vitro, thereby giving rise to hybrid cells with new properties, which likely indicate that cell fusion may be a trigger for tumor heterogeneity. Full article
(This article belongs to the Special Issue Cellular Signalling in Cell Fusion)
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Review

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28 pages, 480 KiB  
Review
Virus-Mediated Cell-Cell Fusion
by Héloïse Leroy, Mingyu Han, Marie Woottum, Lucie Bracq, Jérôme Bouchet, Maorong Xie and Serge Benichou
Int. J. Mol. Sci. 2020, 21(24), 9644; https://doi.org/10.3390/ijms21249644 - 17 Dec 2020
Cited by 71 | Viewed by 9740
Abstract
Cell-cell fusion between eukaryotic cells is a general process involved in many physiological and pathological conditions, including infections by bacteria, parasites, and viruses. As obligate intracellular pathogens, viruses use intracellular machineries and pathways for efficient replication in their host target cells. Interestingly, certain [...] Read more.
Cell-cell fusion between eukaryotic cells is a general process involved in many physiological and pathological conditions, including infections by bacteria, parasites, and viruses. As obligate intracellular pathogens, viruses use intracellular machineries and pathways for efficient replication in their host target cells. Interestingly, certain viruses, and, more especially, enveloped viruses belonging to different viral families and including human pathogens, can mediate cell-cell fusion between infected cells and neighboring non-infected cells. Depending of the cellular environment and tissue organization, this virus-mediated cell-cell fusion leads to the merge of membrane and cytoplasm contents and formation of multinucleated cells, also called syncytia, that can express high amount of viral antigens in tissues and organs of infected hosts. This ability of some viruses to trigger cell-cell fusion between infected cells as virus-donor cells and surrounding non-infected target cells is mainly related to virus-encoded fusion proteins, known as viral fusogens displaying high fusogenic properties, and expressed at the cell surface of the virus-donor cells. Virus-induced cell-cell fusion is then mediated by interactions of these viral fusion proteins with surface molecules or receptors involved in virus entry and expressed on neighboring non-infected cells. Thus, the goal of this review is to give an overview of the different animal virus families, with a more special focus on human pathogens, that can trigger cell-cell fusion. Full article
(This article belongs to the Special Issue Cellular Signalling in Cell Fusion)
13 pages, 975 KiB  
Review
Altered Tumor Plasticity after Different Cancer Cell Fusions with MSC
by Catharina Melzer, Juliane von der Ohe and Ralf Hass
Int. J. Mol. Sci. 2020, 21(21), 8347; https://doi.org/10.3390/ijms21218347 - 6 Nov 2020
Cited by 22 | Viewed by 3143
Abstract
While cell fusion demonstrates an important pathway during tissue development and regeneration of distinct organs, this process can also contribute to pathophysiological phenotypes during tumor progression. Hybrid cell formation after heterofusion between cancer cells and various other cell types within the tumor microenvironment [...] Read more.
While cell fusion demonstrates an important pathway during tissue development and regeneration of distinct organs, this process can also contribute to pathophysiological phenotypes during tumor progression. Hybrid cell formation after heterofusion between cancer cells and various other cell types within the tumor microenvironment is observed in vitro and in vivo. In particular, mesenchymal stroma/stem-like cells (MSC) perform diverse levels of communication with cancer cells by exhibiting anti- and pro-tumorigenic effects. During these cellular interactions, MSC can eventually fuse with cancer cells. Thereby, the newly generated disparate hybrid populations display aneuploidy associated with chromosomal instability. Based upon a subsequent post-hybrid selection process (PHSP), fused cancer cells can undergo apoptosis/necroptosis, senescence, dormancy, or a proliferative state by acquisition of new properties. Consequently, PHSP-surviving hybrid cancer cells demonstrate altered functionalities within the tumor tissue. This is accompanied by changes in therapeutic responsiveness and a different metastatic behavior. Accordingly, enhanced tumor plasticity interferes with successful therapeutic interventions and aggravates patient prognoses. The present review article focusses on fusion of MSC with different human cancer cells, in particular breast cancer populations and resulting characteristics of various cancer hybrid cells. Moreover, some mechanisms of cancer cell fusion are discussed together with multiple PHSP pathways. Full article
(This article belongs to the Special Issue Cellular Signalling in Cell Fusion)
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