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Interaction of MSC with tumor cells

View Article: PubMed Central - PubMed

ABSTRACT

Tumor development and tumor progression is not only determined by the corresponding tumor cells but also by the tumor microenvironment. This includes an orchestrated network of interacting cell types (e.g. immune cells, endothelial cells, fibroblasts, and mesenchymal stroma/stem cells (MSC)) via the extracellular matrix and soluble factors such as cytokines, chemokines, growth factors and various metabolites. Cell populations of the tumor microenvironment can interact directly and indirectly with cancer cells by mutually altering properties and functions of the involved partners. Particularly, mesenchymal stroma/stem cells (MSC) play an important role during carcinogenesis exhibiting different types of intercellular communication. Accordingly, this work focusses on diverse mechanisms of interaction between MSC and cancer cells. Moreover, some functional changes and consequences for both cell types are summarized which can eventually result in the establishment of a carcinoma stem cell niche (CSCN) or the generation of new tumor cell populations by MSC-tumor cell fusion.

No MeSH data available.


Related in: MedlinePlus

Direct interactions between mesenchymal stroma/stem cells and cancer cells. a Notch signaling: A prominent example for direct cell-to-cell interaction is represented by Notch signaling. DAPT, a Notch signaling inhibitor, was shown to decrease functional alterations of breast cancer cells after co-culture with MSC underlining the involvement of Notch signaling in MSC-cancer cell interactions. b GJIC: Both MSC and cancer cells build gap junctions for intercellular communication. Gap junctional intercellular communication (GJIC) can be inhibited by gap junction inhibitor carbenoxolone (CBX) resulting in lesser interactions and functional alterations of cancer cells and MSC. c Nanotube formation: Long and thin plasma membrane structures formed between MSC and cancer cells allow the transport of small molecules and organelles for cellular cross-talk leading to altered functions and phenotype. d Trogocytosis: An exchange of whole plasma membrane fragments via an active transfer outlines a further possible interaction type between MSC and cancer cells resulting in structural and functional alterations of the recipient cell. e Cell fusion: In rare cases, mesenchymal stem cells have the capacity to fuse with various cancer cell types such as breast, ovarian, lung and gastric cancer cells. The molecular mechanism about the formation of such cancer hybrid cells is still unknown
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Fig2: Direct interactions between mesenchymal stroma/stem cells and cancer cells. a Notch signaling: A prominent example for direct cell-to-cell interaction is represented by Notch signaling. DAPT, a Notch signaling inhibitor, was shown to decrease functional alterations of breast cancer cells after co-culture with MSC underlining the involvement of Notch signaling in MSC-cancer cell interactions. b GJIC: Both MSC and cancer cells build gap junctions for intercellular communication. Gap junctional intercellular communication (GJIC) can be inhibited by gap junction inhibitor carbenoxolone (CBX) resulting in lesser interactions and functional alterations of cancer cells and MSC. c Nanotube formation: Long and thin plasma membrane structures formed between MSC and cancer cells allow the transport of small molecules and organelles for cellular cross-talk leading to altered functions and phenotype. d Trogocytosis: An exchange of whole plasma membrane fragments via an active transfer outlines a further possible interaction type between MSC and cancer cells resulting in structural and functional alterations of the recipient cell. e Cell fusion: In rare cases, mesenchymal stem cells have the capacity to fuse with various cancer cell types such as breast, ovarian, lung and gastric cancer cells. The molecular mechanism about the formation of such cancer hybrid cells is still unknown

Mentions: Different types of cross-talk between MSC and cancer cells both directly and indirectly are illustrated in Figs. 1 and 2, respectively. Several direct and/or indirect mechanisms of interaction contribute to MSC-mediated stimulation of cancer cell growth including Notch signaling, nanotube formation, gap junctional intercellular communication, and/or the exchange of cytokines/chemokines, extracellular vesicles and exosomes [36–38]. It is thus important to emphasize that these different types of indirect and direct interactions are always multidirectional, therefore affecting and altering both, the tumor cells as well as the MSC or other cellular partners.Fig. 1


Interaction of MSC with tumor cells
Direct interactions between mesenchymal stroma/stem cells and cancer cells. a Notch signaling: A prominent example for direct cell-to-cell interaction is represented by Notch signaling. DAPT, a Notch signaling inhibitor, was shown to decrease functional alterations of breast cancer cells after co-culture with MSC underlining the involvement of Notch signaling in MSC-cancer cell interactions. b GJIC: Both MSC and cancer cells build gap junctions for intercellular communication. Gap junctional intercellular communication (GJIC) can be inhibited by gap junction inhibitor carbenoxolone (CBX) resulting in lesser interactions and functional alterations of cancer cells and MSC. c Nanotube formation: Long and thin plasma membrane structures formed between MSC and cancer cells allow the transport of small molecules and organelles for cellular cross-talk leading to altered functions and phenotype. d Trogocytosis: An exchange of whole plasma membrane fragments via an active transfer outlines a further possible interaction type between MSC and cancer cells resulting in structural and functional alterations of the recipient cell. e Cell fusion: In rare cases, mesenchymal stem cells have the capacity to fuse with various cancer cell types such as breast, ovarian, lung and gastric cancer cells. The molecular mechanism about the formation of such cancer hybrid cells is still unknown
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC5016940&req=5

Fig2: Direct interactions between mesenchymal stroma/stem cells and cancer cells. a Notch signaling: A prominent example for direct cell-to-cell interaction is represented by Notch signaling. DAPT, a Notch signaling inhibitor, was shown to decrease functional alterations of breast cancer cells after co-culture with MSC underlining the involvement of Notch signaling in MSC-cancer cell interactions. b GJIC: Both MSC and cancer cells build gap junctions for intercellular communication. Gap junctional intercellular communication (GJIC) can be inhibited by gap junction inhibitor carbenoxolone (CBX) resulting in lesser interactions and functional alterations of cancer cells and MSC. c Nanotube formation: Long and thin plasma membrane structures formed between MSC and cancer cells allow the transport of small molecules and organelles for cellular cross-talk leading to altered functions and phenotype. d Trogocytosis: An exchange of whole plasma membrane fragments via an active transfer outlines a further possible interaction type between MSC and cancer cells resulting in structural and functional alterations of the recipient cell. e Cell fusion: In rare cases, mesenchymal stem cells have the capacity to fuse with various cancer cell types such as breast, ovarian, lung and gastric cancer cells. The molecular mechanism about the formation of such cancer hybrid cells is still unknown
Mentions: Different types of cross-talk between MSC and cancer cells both directly and indirectly are illustrated in Figs. 1 and 2, respectively. Several direct and/or indirect mechanisms of interaction contribute to MSC-mediated stimulation of cancer cell growth including Notch signaling, nanotube formation, gap junctional intercellular communication, and/or the exchange of cytokines/chemokines, extracellular vesicles and exosomes [36–38]. It is thus important to emphasize that these different types of indirect and direct interactions are always multidirectional, therefore affecting and altering both, the tumor cells as well as the MSC or other cellular partners.Fig. 1

View Article: PubMed Central - PubMed

ABSTRACT

Tumor development and tumor progression is not only determined by the corresponding tumor cells but also by the tumor microenvironment. This includes an orchestrated network of interacting cell types (e.g. immune cells, endothelial cells, fibroblasts, and mesenchymal stroma/stem cells (MSC)) via the extracellular matrix and soluble factors such as cytokines, chemokines, growth factors and various metabolites. Cell populations of the tumor microenvironment can interact directly and indirectly with cancer cells by mutually altering properties and functions of the involved partners. Particularly, mesenchymal stroma/stem cells (MSC) play an important role during carcinogenesis exhibiting different types of intercellular communication. Accordingly, this work focusses on diverse mechanisms of interaction between MSC and cancer cells. Moreover, some functional changes and consequences for both cell types are summarized which can eventually result in the establishment of a carcinoma stem cell niche (CSCN) or the generation of new tumor cell populations by MSC-tumor cell fusion.

No MeSH data available.


Related in: MedlinePlus