From hydra to human: in silico investigation of the atavistic model of cancer
Öz
Purpose: Cancer manifests as a disruption in the regular functioning of multicellular systems, arising from the malfunctioning of genes responsible for cellular cooperation. Notably, cancer exhibits atavistic characteristics, wherein cancer cells diverge from the conventional Darwinian evolution, highlighting a distinctive trajectory in their evolutionary fate. In this context, cancer cells may display traits such as uncontrolled proliferation, evasion of cell death mechanisms and altered metabolism, which could reflect ancient biological programs related to cell growth and survival. The objective of this study was to trace the evolutionary origin of cancer by analyzing tumor-related proteins in the basal metazoan Hydra and their preservation across diverse taxa.
Materials and Methods: Bioinformatic approaches were employed to investigate the conservation status of protein-coding transcripts that are differentially expressed in the tumor-bearing Hydra across species, representing both unicellular and multicellular forms of life.
Results: By examining the taxonomic distribution of the Hydra polyp-related proteins, we have traced the ancient evolutionary roots of cancer through the tree of life. The majority of protein-coding genes were found to be of unicellular origin and associated with cancer.
Conclusion: We suggest conservation of the atavistic in model of cancer the basal tumor-bearing animals, which can be considered as promising and intriguing candidate model organisms in cancer research.
Anahtar Kelimeler
cancer, atavistic hypothesis, Hydra, phylostratigraphy, bioinformatics
Etik Beyan
We declare there is no conflict of interest
Kaynakça
- Aktipis CA, Nesse RM. Evolutionary foundations for cancer biology. Evol Appl. 2013;6:144-59.
- Rokas A. The origins of multicellularity and the early history of the genetic toolkit for animal development. Annu Rev Genet. 2008;42:235-51.
- Grosberg RK, Strathmann RR. The evolution of multicellularity: a minor major transition? Annual Review of Ecology, Evolution and Systematics. 2007;38:621-54.
- Nedelcu AM. The evolution of multicellularity and cancer: views and paradigms. Biochem Soc Trans. 2020;48:1505-18.
- Aktipis CA, Boddy AM, Jansen G, Hibner U, Hochberg ME, Maley CC et al. Cancer across the tree of life: cooperation and cheating in multicellularity. Philos Trans R Soc Lond B Biol Sci. 2015;370.
- Davies PC, Lineweaver CH. Cancer tumors as Metazoa 1.0: tapping genes of ancient ancestors. Phys Biol. 2011;8:015001.
- Domazet-Loso T, Tautz D. Phylostratigraphic tracking of cancer genes suggests a link to the emergence of multicellularity in metazoa. BMC Biol. 2010;8:66.
- Lineweaver CH, Bussey KJ, Blackburn AC, Davies PCW. Cancer progression as a sequence of atavistic reversions. Bioessays. 2021;43:e2000305.
- Trigos AS, Pearson RB, Papenfuss AT, Goode DL. Altered interactions between unicellular and multicellular genes drive hallmarks of transformation in a diverse range of solid tumors. Proc Natl Acad Sci U S A. 2017;114:6406-11.
- Louka A, Takan I, Pavlopoulou A, Georgakilas AG. Bioinformatic approaches to the investigation of the atavistic genes implicated in cancer. Front Biosci (Landmark Ed). 2021;26:279-311.
