In an adult human body, somatic stem cells are present in small amounts in almost all organs with the function of general maintenance and prevention of premature aging. But, these stem cells are not pluripotent and are unable to regenerate large cellular loss caused by infarctions or fractures especially in cells with limited replicative ability such as neurons and cardiomyocytes. These limitations gave rise to the idea of inducing pluripotency to adult somatic cells and thereby restoring their regeneration, replication and plasticity. Though many trials and research were focused on inducing pluripotency, a solid breakthrough was achieved by Yamanaka in 2006. Yamanaka's research identified 4 genes (OCT-4, SOX-2, KLF-4 and c-MYC) as the key requisite for inducing pluripotency in any somatic cells (iPSCs). Our study, reviews the major methods used for inducing pluripotency, differentiation into specific cell types and their application in both cell regeneration and disease modelling. We have also highlighted the current status of iPSCs in clinical applications by analysing the registered clinical trials. We believe that this review will assist the researchers to decide the parameters such as induction method and focus their efforts towards clinical application of iPSCs.

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Studies conducted in the past decade have reported nucleostemin (NS) as a nucleolar protein that has a role in self-renewal and cell cycle regulation in cancer/stem cells, but is absent in differentiated cells. The localization and expression patterns of NS have always been disputed, as reports indicate its varied levels among tissues and cells. This study evaluates the expression and localization pattern of NS in normal cells, cancer cell lines, and stem cells. Our findings revealed that the expression of NS was high in cancers originating from the skin and liver compared to the normal cell lines. NS knockdown affects the proliferation of normal cell lines, similar to cancerous cell lines. The localization pattern of NS was analyzed by immunofluorescence, which showed that NS was localized in the nuclei of normal cell lines but is present both in the nucleus and the cytoplasm of cancerous/stem cell lines. Interestingly, we observed that siNS cancerous cell lines had lower NS in the cytoplasm, which did not salvage the reduction in proliferation caused by siNS. We postulate that the loss of NS in the nucleus inhibits the proliferative ability of both normal and cancerous cells at similar rates, although the role of NS in the cytoplasm apart from proliferation needs to be further explored.