Unraveling the Significance of Nanog in the Generation of Embryonic Stem-like Cells from Spermatogonia Stem Cells: A Combined In Silico Analysis and In Vitro Experimental Approach.

Embryonic stem-like cells (ES-like cells) are promising for medical research and clinical applications. Traditional methods involve "Yamanaka" transcription (OSKM) to derive these cells from somatic cells in vitro. Recently, a novel approach has emerged, obtaining ES-like cells from spermatogonia stem cells (SSCs) in a time-related process without adding artificial additives to cell cultures, like transcription factors or small molecules such as pten or p53 inhibitors. This study aims to investigate the role of the Nanog in the conversion of SSCs to pluripotent stem cells through both in silico analysis and in vitro experiments. We used bioinformatic methods and microarray data to find significant genes connected to this derivation path, to construct PPI networks, using enrichment analysis, and to construct miRNA-lncRNA networks, as well as in vitro experiments, immunostaining, and Fluidigm qPCR analysis to connect the dots of Nanog significance. We concluded that Nanog is one of the most crucial differentially expressed genes during SSC conversion, collaborating with critical regulators such as Sox2, Dazl, Pou5f1, Dnmt3, and Cdh1. This intricate protein network positions Nanog as a pivotal factor in pathway enrichment for generating ES-like cells, including Wnt signaling, focal adhesion, and PI3K-Akt-mTOR signaling. Nanog expression is presumed to play a vital role in deriving ES-like cells from SSCs in vitro. Finding its pivotal role in this path illuminates future research and clinical applications.

Exploring Myc puzzle: Insights into cancer, stem cell biology, and PPI networks.

"The grand orchestrator," "Universal Amplifier," "double-edged sword," and "Undruggable" are just some of the Myc oncogene so-called names. It has been around 40 years since the discovery of the Myc, and it remains in the mainstream of cancer treatment drugs. Myc is part of basic helix-loop-helix leucine zipper (bHLH-LZ) superfamily proteins, and its dysregulation can be seen in many malignant human tumors. It dysregulates critical pathways in cells that are connected to each other, such as proliferation, growth, cell cycle, and cell adhesion, impacts miRNAs action, intercellular metabolism, DNA replication, differentiation, microenvironment regulation, angiogenesis, and metastasis. Myc, surprisingly, is used in stem cell research too. Its family includes three members, MYC, MYCN, and MYCL, and each dysfunction was observed in different cancer types. This review aims to introduce Myc and its function in the body. Besides, Myc deregulatory mechanisms in cancer cells, their intricate aspects will be discussed. We will look at promising drugs and Myc-based therapies. Finally, Myc and its role in stemness, Myc pathways based on PPI network analysis, and future insights will be explained.