Abstract
X chromosome inactivation is the epitome of epigenetic regulation and long non-coding ribonucleic acid function. The differentiation status of cells has been ascribed to X chromosome activity, with two active X chromosomes generally only observed in undifferentiated or poorly differentiated cells. Recently, several studies have indicated that the reactivation of an inactive X chromosome or X chromosome multiplication correlates with the development of malignancy; however, this concept is still controversial. This review sought to shed light on the role of the X chromosome in cancer development. In particular, there is a need for further exploration of the expression patterns of X-linked genes in cancer cells, especially those in head and neck squamous cell carcinoma (HNSCC), in order to identify different prognostic subpopulations with distinct clinical implications. This article proposes a functional relationship between the loss of the Barr body and the disproportional expression of X-linked genes in HNSCC development.
Highlights
X chromosome inactivation is the epitome of epigenetic regulation and long non-coding ribonucleic acid function
There is a need for further exploration of the expression patterns of X-linked genes in cancer cells, especially those in head and neck squamous cell carcinoma (HNSCC), in order to identify different prognostic subpopulations with distinct clinical implications
The exclusivity of tumour suppressor genes (TSGs) to the X chromosome can be attributed to their inactivation by a single referred loss of function mutation; in other words, if a tumour suppressor gene is localised on the X chromosome, one hit is sufficient to induce tumorigenesis because the other allele on the X chromosome is inactivated by epigenetic modification
Summary
Abstract: X chromosome inactivation is the epitome of epigenetic regulation and long non-coding ribonucleic acid function. Genetic and epigenetic processes result in heritable changes in the expression of cancer cells; the molecular targets of malignancy include critical tumour-associated genes—such as tumour suppressor genes (TSGs) or oncogenes—along with their mutations, amplifications, deletions, loss of heterozygosity or other epigenetic modifications.[1] Recently, researchers have confirmed the role of DNA methylation and histone modification of the cytosine-guanine (CpG) site in malignancy as well as the interrelation between nuclear architecture, chromatin packaging, heterochromatin organisation, epigenome and noncoding ribonucleic acid (RNA).[2] Many X-linked potential TSGs and oncogenes have been attributed to the distinctive biology of the X chromosome and its specific implications in malignancy.[3] The exclusivity of TSGs to the X chromosome can be attributed to their inactivation by a single referred loss of function mutation (i.e. hit); in other words, if a tumour suppressor gene is localised on the X chromosome, one hit is sufficient to induce tumorigenesis because the other allele on the X chromosome is inactivated by epigenetic modification. There is a need to further explore the role of sex chromosomes in HNSCC development in order to determine potential clinical implications
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