OCT4, SOX2 and NANOG co-regulate glycolysis and participate in somatic induced reprogramming
OCT4, SOX2 and NANOG (OSN) are the key factors of cell reprogramming, which are involved in the maintenance of stem cell pluripotency. Recently, it has been found that glycolysis plays an important role in the process of somatic-cell-induced reprogramming; however, the synergistic effect of OSN on g...
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Published in | Cytotechnology (Dordrecht) Vol. 74; no. 3; pp. 371 - 383 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Dordrecht
Springer Netherlands
01.06.2022
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | OCT4, SOX2 and NANOG (OSN) are the key factors of cell reprogramming, which are involved in the maintenance of stem cell pluripotency. Recently, it has been found that glycolysis plays an important role in the process of somatic-cell-induced reprogramming; however, the synergistic effect of OSN on glycolysis has rarely been reported. In this study, chicken embryonic fibroblasts (CEF) was reprogrammed into induced pluripotent stem cells (iPSCs) by OCT4, SOX2, NANOG and LIN28 reprogramming strategy. RNA-seq showed that chicken iPSCs highly expressed pluripotent genes and the expression of the key genes of glycolysis, such as
Hk1, Pfkp
and
Ldha
, was also at a high level, while CEF was much lower. Glycolysis gene expression, glucose uptake and lactate production of CEF and iPSCs were also detected. The results showed that the glycolysis level of iPSCs was higher than that of CEF. ChIP-qPCR showed that SOX2 and NANOG transcription factors were significantly enriched in the promoter regions of
Hk1, Pfkp
and
Ldha
, while OCT4 was not. The above results indicated that OCT4, SOX2 and NANOG coordinately regulate glycolysis and participate in somatic-cell-induced reprogramming, thus setting a good foundation for further research on the molecular mechanism of somatic-cell-induced reprogramming. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0920-9069 1573-0778 |
DOI: | 10.1007/s10616-022-00530-6 |