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NANOG is the human ortholog of the mouse Nanog gene1 and is a member of the homeobox family of DNA binding transcription factors.2 NANOG plays an important role in the maintenance of pluripotency and self-renewal of human embryonic stem cells.3 ,4
Chambers et al 3 were the first researchers who identified this transcription factor and named it according to the mythological Celtic land of the ever young, Tír na nÓg. Their study was focussed on comparing expressed sequence tag (ESC) libraries between mouse ESCs and various somatic tissues. They also detected this gene in the mouse embryonic carcinoma cells.
NANOG is a transcription factor that forms part of a complex regulatory network and its function is based on regulating cell death, proliferation and determining cell fate.5 It is known that NANOG is expressed in cancer stem cells (CSCs) and ESCs.5 Indeed, CSCs have the potential to regulate self-renewal and differentiation within a tumour, triggering tumourigenesis, and NANOG promotes the long-term proliferative potential of these cells.6 Additionally, various studies have suggested that NANOG protein is highly expressed in cancerous tissues, whereas in normal adult tissues, its expression is much lower.5
This short review highlights several aspects of the structure, expression and function of the NANOG gene, including also its role in tumourigenesis and various types of cancers, cancer prognosis and anticancer therapies.
Both the human and murine Nanog gene are located in the short arm of chromosome 12 (12p13), a ‘hotspot’ region frequently exposed to duplications and amplifications in human tumours derived from the germ line, particularly in male germ cell tumours.2 ,7 The human and the mouse Nanog gene encode for a protein of 305 amino acids.2 ,5 ,8 Surprisingly, when comparing the 60 amino acids in …
Handling editor Runjan Chetty
Contributors Study concept and design: AEF and JK; literature review: MMP and AEF; analysis and interpretation of literature: MMP; drafting of the manuscript: AEF and MMP; revision of manuscript: AEF, JK and JS; supervision of work: AEF, JK and JS.
Funding Action Against Cancer.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
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