Novel Pathways of Cell Fate Regulation

Dear Colleagues,

Understanding the molecular mechanisms underlying cell fate, i.e., whether a cell will remain a stem cell, or differentiate, or undergo transformation, etc., is one of the most intricate challenges of modern cell biology.

To study these phenomena, several in vitro and in vivo models were developed. Using them, it was shown that the stemness of the cells is dependent on an expression pattern of a set of transcription factors (TFs). Differentiation might be induced by changes in the TF expression pattern, or by cocktails of certain chemical compounds.

The same is true for cell transformation in general: cells can be transformed by the action of chemicals; by viral proteins; upon changes of genome methylation; and, of course, by gene mutations and chromosomal re-arrangements.

It is accepted that stem and cancerous cells show several similar features, i.e., they are immortal, can proliferate constitutively, show de-differentiated morphology, and have many common activated TFs, for example, C-MYC, KLF4, OCT4, SOX2, etc. An obvious connection between stem and cancerous cells was also shown by S. Yamanaka, by inducing pluripotent stem cells from terminally differentiated fibroblasts by overexpression of the abovementioned proteins.

Despite the progress in the study of molecular mechanisms controlling cell fate, many questions remain unanswered and have not even been formulated yet. For example, why are the cellular pathways, regulated by the retinoblastoma associated protein (RB) that are inactivated during cancerogenesis, not functioning in embryonic stem cells? Importantly, loss of the RB-encoding gene results in the development of specific types of tumors and the embryonic lethality of knock-out mice.

We encourage authors to present their point of view on the alternative mechanisms of regulation of cell fate, and on unexplored problems concerning cell biology.

Dr. Elena Kashuba
Guest Editor

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• cell fate
• stemness
• differentiation
• cancerous cell
• transformation
• immortalization
• transcription factor
• chromosome rearrangement
• methylation