Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 26, Issue 8, Pages 279-311Publisher
IMR PRESS
DOI: 10.52586/4944
Keywords
Atavism; Cancer; Bioinformatics; Evolution; Phylogeny; Biological pathways; Unicellularity; Multicel-lularity
Categories
Funding
- YOK (Yuksekogretim Kurulu) scholarship
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This study utilized bioinformatic approaches to investigate twelve atavistic hub genes associated with disrupted interactions in various types of cancer, revealing that most of these genes originate from unicellular organisms and some can be traced back to the emergence of cellular life itself. The findings highlight the deep evolutionary roots of cancer and suggest potential applications in designing novel therapeutic approaches to overcome resistance to anticancer treatment in clinical settings.
Introduction: Cancer is a widespread phenomenon occurring across multicellular organisms and represents a condition of atavism, wherein cells follow a path of reverse evolution that unlocks a toolkit of ancient preexisting adaptations by disturbing hub genes of the human gene network. This results to a primitive cellular phenotype which resembles a unicellular life form. Methods: In the present study, we have employed bioinformatic approaches for the in-depth investigation of twelve atavistic hub genes (ACTG1, CTNNA1, CTNND1, CTTN, DSP, ILK, PKN2, PKP3, PLEC, RCC2, TLN1 and VASP), which exhibit highly disrupted interactions in diverse types of cancer and are associated with the formation of metastasis. To this end, phylogenetic analyses were conducted towards unravelling the evolutionary history of those hubs and tracing the origin of cancer in the Tree of Life. Results: Based on our results, most of those genes are of unicellular origin, and some of them can be traced back to the emergence of cellular life itself (atavistic theory). Our findings indicate how deep the evolutionary roots of cancer actually are, and may be exploited in the clinical setting for the design of novel therapeutic approaches and, particularly, in overcoming resistance to antineoplastic treatment.
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