Figure 10

ADSC modulate angiogenesis in CC tumors. (a) Graph shows the fold increase of DE mRNAs involved in angiogenesis obtained from HeLa/ADSC RNAseq data. Angiogenesis-related mRNAs shown are VEGF-C, and CXCL2. (b) Representative network of KPA analysis showing that NF-Kappa B/VEGF-C activates the signaling of angiogenic factors in HeLa cells cocultured in the presence of ADSC. (c) Representative photograph of the infiltration of SiHa cells in the blood vessels of fli1a embryos: EGFP after 12 h post-injection is shown. The SiHa cells are observed in red color and blood vessels in green. (d) Representative figure showing the formation of new blood vessels in the yolk of embryos from day 1 dpi and 3 dpi of SiHa cells vs SiHa-ADSC. (e) The illustration built with the experimental data obtained, indicates that the ADSCs migrate from the adipose tissue to CC tumor and there, they increase the malignant phenotype of the CC cells and promoting metastasis. The ADSC potentiate the malignant phenotype of cervical cancer cells by increasing the non-canonical NF-Kappa B pathway, causing an increase in the expression of chemokines, transcription factors, metalloproteases, integrins, etc., which contribute to the increased migration and invasion capacity of cancer cells. In addition, ADSC activate the EMT process mainly due to the increase of Fibronectin in CC cells. Finally, ADSCs induce the angiogenic potential that plays an important role in tumor progression. It should be mentioned that all these phenotypic changes could be given by the activation of the NF-Kappa B pathway.