ISSN: 2640-2637
Authors: Roman Anton*
Embryonic stem cells (ESCs) and induced pluripotent stem cell (iPSCs), which are somatic body cells reprogrammed into ESCs, are powerful sources of regenerative medicine. iPSCs and ESCs pluripotency have the capacity to enable all cellular and organ strategies for regenerative replacement and rejuvenation therapy. This unique ability to differentiate into all cell types and tissues of the body is maintained if they are propagated under self-renewal culture conditions, which sustains the molecular basis of pluripotency by maintaining transcriptional and epigenetic mechanism of stemness in ESCs and iPSCs inter alia. This auto-equilibrated pluripotency transcriptional circuitis the result of a network of key transcription factors that globally organizes the stemness of the genome, transcriptome, and proteome. A self-sustaining transcriptional network of transcriptional activators and repressors that reinforce themselves and other factors comprises the important master regulators Oct-3/4, Nanog, Sox-2, and KLf-4. These factors globally coordinate genomic gene expression and are of a highest functional-regulatory order that even allows the reprogramming of specialized body cells into iPSCs. The mechanistic logic behind stemness will also help to decode cell identity and the program of all cells and is a long-standing research objective of regenerative medicine, iPSC biomedicine development, and a new organizational challenge for system biology and open science. The stemness network has adjacent biomarker and regulator states. Understanding the mechanistic logic behind all of the steps can help to engineer different cellular states to produce adult stem cells or specialized biomedical cells and can help to heal inherited or acquired diseases such as cancer. Stemness factor equilibrium in ESCs is stabilized in circuits by signaling, cellular context, and culture conditions. This work re-proposes a systems biology approach using open platforms of systematic GOF and LOF cell line comparisons and delivers a proof-of-principal concept for a big open systems biology approach. By dissecting the role of Wnt/β-catenin signaling in stemness, new non-TCF and new E-cadherin-dependent functions emerge.
Keywords: Escs; Ipscs; Oct3/4; Nanog; KLF-; Sox; Stemness; Beta-Catenin; CTNNB1; Cadherin; Stem Cells; Maintenance; Lif; Pluripotency; Wnt; Signaling; Systems Biology; Biomarker; Open Science; Cdh1; E-Cadherin; Cell Adhesion; Rex-1; TERT; Transcription; Factor; Network; Reprogramming; Biomedicine; Regenerative Medicine; Tissue, Cell; Engineering; Organ Replacement; Cell Fate; Cell Identity; Circuits
