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Cancer Stem Cells 2019 Journal of Medical Oncology andTherapeutics | Volume 4
July 18-19, 2019 | Valencia, Spain
OF EXCELLENCE
IN INTERNATIONAL
MEETINGS
YEARS
CANCER STEM CELLS AND
ONCOLOGY RESEARCH
12th International Conference on
CANCER STEM CELLS DEDIFFERENTIATION AS THE CORNERSTONE OF TUMOR RE-
LAPSE AND DISEASE PROGRESSION
Carlos FD Rodrigues1,2,3, Eurico Serrano1,2, Patrícia Albuquerque1,4, Luís Almeida1,4 and
Maria Carmen Alpoim1,2,5
1 Center for Neuroscience and Cell Biology (CNC), University of Coimbra, Portugal
2 Center of Investigation in Environment, Genetics and Oncobiology (CIMAGO), University of Coimbra, Portugal
3 Centro Hospitalar do Baixo Vouga, Portugal
4 Faculty of Pharmacy (FFUC), University of Coimbra, Portugal
5 Department of Life Sciences, University of Coimbra, Portugal
C ancer stem cells (CSCs) are the orchestrators of the intricate communication pathways hijacked by tumors
to overcome the inefficiency of the invasion-metastasis cascade. Their plasticity and boosted defense
mechanisms permits their survival to the current therapeutic regimens, thus retaining the potential to drive
tumor relapse. After observing that the malignant human bronchial epithelial RenG2 cells dedifferentiated
following culture in the subcutaneous mouse lumbar region, co-cultures of mice lumbar fibroblats with RenG2
cells were established and the conditioned media was studied. Results showed Interleukin-6 (IL-6), Granulocyte
colony-stimulating factor (G-CSF) and Activin-A were the mediators of the aforementioned intercellular com-
munication process, which prompted the study of the individual role of each cytokine and of exosomes in the
overall process. To this end the same co-cultures were reproduced in the presence of combinations of specific
cytokine-communication blockers and exosome-mediated communication inhibitors. Whenever exosome’s
release was blocked, dedifferentiation was abrogated. Additionally, only IL-6 and Activin-A were endowed with
the potential to orchestrate dedifferentiation, as when at least one of these cytokines was present a stem cell
population developed inside RenG2 cells. G-CSF only maintained CSC’s undifferentiated phenotype, as a larger
pool of CSCs was attained whenever this cytokine and either IL-6 or Activin-A was present. The attained results
implicated IL-6 and Activin-A in the formation of CSCs by dedifferentiation and G-CSF as a potent keeper of the
dedifferentiation status. The scavenging of these cytokines from the tumor microenvironment presents a new
avenue for therapeutic intervention aiming CSCs ablation and metastasis abrogation.
Carlos FD Rodrigues et al., J Med Oncl Ther 2019, Volume 4
Carlos FD Rodrigues has been graduated from the University of Coimbra, Portugal as both Medical Doctor and a Biologist. He holds
a PhD in Biomedicine and Experimental Biology and a Master in Medicine from the same university. Currently he is taking his spe-
cialization in Internal Medicine in the Centro Hospitalar do Baixo Vouga, Portugal while continuing his research both at his Hospital
in Aveiro and at the Center for Neuroscience and Cellular Biology in Coimbra, Portugal.
BIOGRAPHY