Murine melanoma cells incomplete reprogramming using non‐viral vector

Câmara, Diana Aparecida Dias; Porcacchia, Allan Saj; Costa, André Santos; Azevedo, Ricardo A.; Kerkis, Irina

doi:10.1111/cpr.12352

Cited by 7 publications

(8 citation statements)

References 47 publications

(48 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Here, cells show similar morphology to iPS cells and expression of pluripotency markers, but no teratoma formation in vivo. However, subsequent tumors were smaller compared to tumors obtained upon injecting the parental B16F10 cells due to the decrease in proliferative capacity of the partially reprogrammed cells, which reduces aggressiveness of tumors and supports the increment in cancer plasticity and melanoma phenotype switching [92].…”

Section: Partial Reprogramming Of Melanoma Cellsmentioning

confidence: 82%

“…Non-viral methods have also been used to partially reprogram murine melanoma cells for 12 to 18 days, using four transcription factors: Oct4, Sox2, Lin28 and Nanog [92]. In this method, Câmara and collaborators (2017) transformed melanoma cells into less aggressive murine melanoma cancer cells.…”

Section: Partial Reprogramming Of Melanoma Cellsmentioning

confidence: 99%

“…Today's therapeutic options for the treatment of metastatic melanoma are still not efficient enough to avoid recurrence mostly because of the development of resistances. Combination Non-viral methods have also been used to partially reprogram murine melanoma cells for 12 to 18 days, using four transcription factors: Oct4, Sox2, Lin28 and Nanog [92]. In this method, Câmara and collaborators (2017) transformed melanoma cells into less aggressive murine melanoma cancer cells.…”

Section: Partial Reprogramming Of Melanoma Cellsmentioning

confidence: 99%

See 2 more Smart Citations

Cellular Reprogramming—A Model for Melanoma Cellular Plasticity

Granados

Poelchen

Novak

et al. 2020

IJMS

View full text Add to dashboard Cite

Cellular plasticity of cancer cells is often associated with phenotypic heterogeneity and drug resistance and thus remains a major challenge for the treatment of melanoma and other types of cancer. Melanoma cells have the capacity to switch their phenotype during tumor progression, from a proliferative and differentiated phenotype to a more invasive and dedifferentiated phenotype. However, the molecular mechanisms driving this phenotype switch are not yet fully understood. Considering that cellular heterogeneity within the tumor contributes to the high plasticity typically observed in melanoma, it is crucial to generate suitable models to investigate this phenomenon in detail. Here, we discuss the use of complete and partial reprogramming into induced pluripotent cancer (iPC) cells as a tool to obtain new insights into melanoma cellular plasticity. We consider this a relevant topic due to the high plasticity of melanoma cells and its association with a strong resistance to standard anticancer treatments.

show abstract

Section: Partial Reprogramming Of Melanoma Cellsmentioning

confidence: 82%

Section: Partial Reprogramming Of Melanoma Cellsmentioning

confidence: 99%

Section: Partial Reprogramming Of Melanoma Cellsmentioning

confidence: 99%

See 1 more Smart Citation

Cellular Reprogramming—A Model for Melanoma Cellular Plasticity

Granados

Poelchen

Novak

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…In an interesting development for cancer treatment, minicircles were used to reprogram murine melanoma cells. The reprogramed cancer cells were less malignant than non-reprogrammed cancer cells, as evidenced by a smaller proportion of cells in S-phase and by the formation of smaller tumors in mice [ 59 ].…”

Section: Using Minimized Dna Vectors For Stem Cell Therapy and Stem Cell Reprogrammingmentioning

confidence: 99%

Improving therapeutic potential of non-viral minimized DNA vectors

Arévalo-Soliz¹,

Hardee²,

Fogg³

et al. 2020

Cell Gene Therapy Insights

View full text Add to dashboard Cite

The tragic deaths of three patients in a recent AAV-based X-linked myotubular myopathy clinical trial highlight once again the pressing need for safe and reliable gene delivery vectors. Non-viral minimized DNA vectors offer one possible way to meet this need. Recent pre-clinical results with minimized DNA vectors have yielded promising outcomes in cancer therapy, stem cell therapy, stem cell reprograming, and other uses. Broad clinical use of these vectors, however, remains to be realized. Further advances in vector design and production are ongoing. An intriguing and promising potential development results from manipulation of the specific shape of non-viral minimized DNA vectors. By improving cellular uptake and biodistribution specificity, this approach could impact gene therapy, DNA nanotechnology, and personalized medicine.

show abstract

“…Nevertheless, the data are provocative, since they so clearly suggest that the assumption that PD-1 blockade works solely by reversing the exhausted phenotype of TILs is not supported by the real-life patient data. This may not be entirely surprising, given the data characterizing the epigenetic changes in exhausted T cells suggest that it may not be so easy to reinvigorate this phenotype (Ca ˆmara et al, 2017;Pauken et al, 2016). In addition, the role of the PD-1 pathway in mediating inhibitory crosstalk between T cells and antigen-presenting cells supports the notion that some of the therapeutic effect of PD-1 pathway blockade may rationally result from dis-inhibition occurring outside of the tumor microenvironment.…”

mentioning

confidence: 99%