Tumor reversion and embryo morphogenetic factors

Several studies have shown that cancer cells can be phenotypically reversed, thus achieving a tumor reversion, by losing malignant hallmarks as migrating and invasive capabilities. These findings suggest that genome activity can switch to assume a different functional configuration, i.e. a different Gene Regulatory Network pattern. Indeed, once destabilized, cancer cells enter into a critical transition phase that can be adequately oriented by yet unidentified morphogenetic factors - acting on both cells and their microenvironment - that trigger an orchestrated array of structural and epigenetic changes. Such process can bypass genetic abnormalities, through rerouting cells toward a benign phenotype. Oocytes and embryonic tissues, obtained by animals and humans, display such reprogramming capability, as a number of yet scarcely identified embryo-derived factors can revert the malignant phenotype of several types of tumors. Mechanisms involved in the reversion process include the modification of cell-microenvironment cross talk (mostly through cytoskeleton reshaping), chromatin opening, demethylation, and epigenetic changes, modulation of biochemical pathways, comprising TCTP-p53, PI3K-AKT, FGF, Wnt, and TGF-8-dependent cascades. Results herein discussed promise to open new perspectives not only in the comprehension of cancer biology but also toward different therapeutic options, as suggested by a few preliminary clinical studies.

Automated summary

Cancer cells can revert to a benign phenotype by changing their gene regulatory network pattern, involving structural and epigenetic changes and bypassing genetic abnormalities. Embryonic tissues and oocytes have the ability to reprogram cancer cells and revert their malignant phenotype. This study provides new perspectives in understanding cancer biology and potential therapeutic options.