The cells of multicellular organisms are genetically homogeneous but heterogenous in structure and function by virtue of differential gene expression. During embryonic development, differential gene expression by modification of
chromatin (
DNA and
histone complex) regulates the developmental proceedings before and after the germ layers are formed. Post-replicative
DNA modification, where the fifth
carbon atom of the
cytosine gets methylated (hereafter, DNA methylation), does not incorporate mutations within the
DNA. In the past few years, a boom has been observed in the field of research related to various epigenetic regulation models, which includes DNA methylation, post-translational modification of
histone tails, control of
chromatin structure by non-coding RNAs, and remodeling of
nucleosome. Epigenetic effects like DNA methylation or
histone modification play a cardinal role in development but also be able to arise stochastically, as observed during aging, in
tumor development and
cancer progression. Over the past few decades, researchers allured toward the involvement of pluripotency inducer genes in
cancer progression and apparent for
prostate cancer (PCa); also, PCa is the most diagnosed
tumor worldwide and comes to the second position in causing mortality in men. The anomalous articulation of pluripotency-inducing
transcription factor; SRY-related HMG box-containing transcription factor-2 (SOX2), Octamer-binding
transcription factor 4 (OCT4) or
POU domain, class 5, transcription factor 1 (POU5F1), and NANOG have been reported in different
cancers which includes
breast cancer,
tongue cancer, and
lung cancer, etc. Although there is a variety in gene expression signatures demonstrated by
cancer cells, the epigenetic mode of regulation at the pluripotency-associated genes in PCa has been recently explored. This chapter focuses on the epigenetic control of NANOG and SOX2 genes in human PCa and the precise role thereof executed by the two
transcription factors.