Stem cells can replenish their own population while supplying the cells necessary to maintain tissue homeostasis. Pluripotent stem cells, which have broader developmental potency than tissue stem cells, are derived from the same source in mice and humans. We have been analyzing the functions of phosophoinositide-3 kinase (PI3K) and its downstream serine/threonine kinase Akt in a variety of stem cell systems.Primordial germ cells (PGCs), which are embryonic germ cell precursors, are unique in that they acquire pluripotency under cultural and pathological conditions. PGCs lacking Pten, which encodes a phosphatase that antagonizes PI3K signaling, give rise to early-onset testicular teratomas in vivo and augment the derivation of pluripotent embryonic germ (EG) cells in vitro. Transient activation of Akt sufficiently recapitulates the effects of Pten deficiency on EG cell derivation. Enhanced EG cell derivation is brought about by the Akt-mediated inhibition of the tumor suppressor p53. In embryonic stem (ES) cells, PI3K/Akt signaling plays a pivotal role in maintaining pluripotency in part via transcriptional activation of the pluripotent transcription factor Nanog. In turn, the expression of Tcl1, a cofactor of Akt, is activated by pluripotent transcription factors, including Oct- 3/4. Therefore, PI3K/Akt signaling and the transcription factor network constitute the positive feedback circuitry necessary to maintain pluripotency in ES cells.In tissue stem cells, such as hair follicular, intestinal, and hematopoietic stem cells, PI3K/Akt signaling activates quiescent stem cells, leading to the generation of committed progenitors and cancer stem cells. These findings underscore the idea that PI3K/Akt signaling regulates "stemness" in many stem cell systems.

Introduction: Anaplastic thyroid cancer (ATC) is an undifferentiated form of thyroid cancer that is highly lethal. The aim of the current study was to search the microarray libraries available in the National Center for Biotechnology Information (NCBI) and analyze the function of the extracted genes to predict their role in the pathogenesis of ATC.Materials and Methods: The data in the GSE33630 dataset were first analyzed by GEO2R and then by R software version 4.2.0. Normalization of data and extraction of genes with significant expression differences (DEGs) were performed and performance analysis was performed by Enrichr and DAVID 6.8.Results: The analyses showed that 1705 genes with log2FC>1 had increased expression and 2740 genes with log2FC<-1 had decreased expression. Also, the PI3K/Akt signaling pathway and the transcription factors IRF8, TCF4, CBEPB and JUND are related to the increased expressed genes.Conclusion: Increased activity of PI3K-Akt signaling pathway as well as transcription factors IRF8,TCF4, CBEPB and JUND in thyroid cells probably leads to the development or progression of ATC cancer.