Inhibition of
Sox2 transcription has been shown to be required for the progression of neurogenesis in the IE (17).
In a different original study using an immunocytologic approach, Ren and Klump showed that 87.6% of carcinomas of Mullerian origin in ascites and pleural fluids were positive for PAX8; 19.2%, 18.1%, 23.4%, and 8.5% of high-grade serous carcinomas were positive for GATA3,
SOX2, uroplakin II, and SALL4, respectively.
(4-7) Markers of CSCs include Sry-related HMG box (
SOX2) and octamer binding transcription factor 4 (OCT4), which are thought to regulate the apoptosis pathway (via caspase-3), telomerase function (via human telomerase reverse transcription or hTERT), and DNA damage repair (via checkpoint kinase 1 or Chk1).
Previously, the four reprogramming factors --proteins OCT4,
SOX2, KLF4 and cMYC--had to be introduce individually to the cells to induce them to change in the proper fashion for the desired outcome.
Cancer stem cell (CSC) is centered in the Cancer stem cell model of carcinogenesis and this idea is enriched by increased expression of the pluripotent stem cell markers like OCT4,
SOX2, NANOG in HNSCC cell lines and other CSC markers like ABCG2, CD44, and ALDH1 that are proverbial to have tumour-inducing potential.
They focused in part on the gene
Sox2 and its associated protein -- which are already known to trigger esophageal conditions when their function is disrupted.
Asmall-molecule inhibitor of tgf-Beta signaling replaces
sox2 in reprogramming by inducing nanog.
The POU domain-containing Oct4 [10] and the HMG domain-containing
SOX2 are two other transcription factors known to be essential for normal pluripotent cell development and maintenance [11].
The research team targeted two genes that are only expressed in stem cells and known to be integral to pluripotency:
Sox2 and Oct4.
Cluster 1 includes proteins CASP3, CASP9, BAX, TP53, BAD, GSK3B, POU5F1, MAPK14, CREB1,
SOX2, and KLF4.
iPSCs were artificially produced for the first time by Takahashi and Yamanaka through ectopic expression of Oct4,
Sox2, Klf4, and cMyc (together OSKM) in murine somatic cells [4] and by Thompson's group in human cells by replacing Klf4 and cMyc with factors LIN28 and NANOG [5].