Thursday, October 11, 2018

Cancer Stem Cells: Foe or Reprogrammable Cells for Efficient Cancer Therapy?

"The ultimate goal should not be to destroy cancer stem cells, but to differentiate and reprogram them"

Extremely – low frequency pulsed electromagnetic fields (ELF-MF) of 50 HZ, 0.8mTesla (rms), are able to orchestrate stem cell commitment towards one of the most complex embryogenetic outcomes, inducing cardiogenesis in embryonic stem cells [72]. ELF-MF are also able to modulate a cardiogenic program throughout the adulthood, as shown by the ability to increase the expression of genes needed for cardiogenesis and the maintenance of a myocardial phenotype in adult ventricular cardiomyocytes [73].
We have recently shown that asymmetrically conveyed electromagnetic fields (ACEF) of 2.4 GHz optimize the expression of pluripotency in mouse ES cells, inducing myocardial, neuronal and skeletal muscle differentiation [74]. Similar results are obtained upon exposure to ACEF of ADhMSCs [75]. This effect is the result of a fine modulation (initial increase and subsequent transcriptional inhibition) of the expression of stemness related genes [75]. Exposure to ACEF was able to induce a biphasic effect, i.e. overexpression followed by transcriptional inhibition of Sox2, Nanog, Oct3/4, Klf4 and c-myc in human skin fibroblasts, affording for the first time a direct high-yield reprogramming of adult nonstem somatic cells into myocardial, neural and skeletal muscle cells (about 15-20% for each phenotypic commitment) [76].
For the first time, through the exposure to ACEF we were able to reverse the process of stem cell senescence in human adult stem cells (ADhMSCs) subjected to prolonged (30 to 90 days) in vitro expansion [77, 78]. This effect resulted from and was associated with (i) the activation of a telomerase dependent pathway, linked to the re-expression of TERT, the gene coding for the catalytic core of telomerase with subsequent increase in telomere length [77], (ii) the induction of a telomerase independent pathway associated with the activation of Bmi-1 and the transient increase in the expression of pluripotency genes, such as Nanog, Sox2 and Oct4 [77], and (iii) the resumption of multilineage differentiation potential, as shown by recovery of high throughput of differentiation along vasculogenic, osteogenic, and adipogenic fates [78].
On the whole, these findings suggest that electromagnetic fields may have a role not only in the specification but also in the persistence of a complex cellular identity. The ability of electromagnetic fields to drive efficient cardiogenesis in both embryonic and adult stem cells and to reprogram even human skin fibroblasts into myocardial-like cells poses intriguing trans-disciplinary musing. In fact, the heart has the lowest risk for primary malignant transformation, which may very rarely develop in the form of cardiac sarcomas [79-81]. Cardiogenesis is the first morphogenetic event in different animal species, including humans. The risk for tumorigenesis throughout embryo development is also very rare [5-7]. The canonical view speculating that primary cardiac malignant tumors are so rare since cardiac cells divide very rarely appears to be too simplistic. An alternative although nonmutually exclusive hypothesis may consider the heart as a tumor suppressor organ, capable of secreting a large network of growth regulatory and differentiating peptides that may potentially limit the onset and progression of a local cancer. In this regard, the attainment of cardiogenesis in the presence of either chemical agents or physical stimulation encompasses the transcription and protein expression of endorphin peptides [33]. These molecules, besides their role in cardiogenesis [55-57], have long been shown to act as negative regulators for the development and spreading of different types of cancer [82-87].
In isolated (stem) cell nuclei endorphin peptides have been shown to bind and activate nuclear receptors and signaling leading to the transcription of their own coding gene (self-sustaining loop), as well as the transcription of the cardiogenic genes GATA4 and Nkx-2.5 [88, 56]. These findings suggest that a consistent part of the action of these growth factors on stem cell dynamics may have occurred intracellularly (intracrine action) [89, 90]. Cell plasma membrane has long been considered an insuperable barrier for hydrosoluble peptides. The discovery that regulatory peptides and transcription factors can be exchanged among cells being packaged inside exosomes, acting in an intracrine fashion, discloses novel paradigms in cell-to-cell communication and adds further relevance for intracrine regulation of cell biology [90, 91]. We cannot exclude that cardiogenesis, within its morphogenetic role, may act as a paracrine/intracrine process that contributes to make the developing embryo remarkably refractory to cancerogenic risks. Whether exposure of human cancer stem cells to electromagnetic fields may resume the ability to differentiate along a cardiogenic lineage and other differentiation patterns remain to be elucidated. Addressing this issue will require thorough investigation in vitro and in vivo in different animal models for cancerogenesis.
http://jnanoworld.com/articles/v1n3/nwj-010-carlo-ventura.html

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