Ectopic overexpression of Nanog induces tumorigenesis in non-tumorous fibroblasts
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Yo Seph Park
, Judee Grace E. Nemeño , Na Young Choi , Jeong Ik Lee , Kisung Ko , Seung-Cheol Choi , Wan Seop Kim , Dong Wook Han , Natalia Tapia und Kinarm Ko
Abstract
Key regulatory genes in pluripotent stem cells are of interest not only as reprogramming factors but also as regulators driving tumorigenesis. Nanog is a transcription factor involved in the maintenance of embryonic stem cells and is one of the reprogramming factors along with Oct4, Sox2, and Lin28. Nanog expression has been detected in different types of tumors, and its expression is a poor prognosis for cancer patients. However, there is no clear evidence that Nanog is functionally involved in tumorigenesis. In this study, we induced overexpression of Nanog in mouse embryonic fibroblast cells and subsequently assessed their morphological changes, proliferation rate, and tumor formation ability. We found that Nanog overexpression induced immortalization of mouse embryonic fibroblast cells (MEFs) and increased their proliferation rate in vitro. We also found that formation of tumors after subcutaneous injection of retroviral-Nanog infected MEFs (N-MEFs) into athymic mouse. Cancer-related genes such as Bmi1 were expressed at high levels in N-MEFs. Hence, our results demonstrate that Nanog is able to transform normal somatic cells into tumor cells.
Acknowledgments
This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT and Future Planning (2014R1A2A01007212 and 2015M3A9C7030066).
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©2016 by De Gruyter
Artikel in diesem Heft
- Frontmatter
- Guest Editorial
- Highlight: Perspectives of molecular neuroscience in health and disease
- HIGHLIGHT: CURRENT CONCE PTS OF PROTECTION AND REGE NERATION IN BRAIN DISORDERS
- The cytoskeleton as a drug target for neuroprotection: the case of the autism- mutated ADNP
- Protein aggregate formation in oligodendrocytes: tau and the cytoskeleton at the intersection of neuroprotection and neurodegeneration
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- Signaling pathways regulating Homer1a expression: implications for antidepressant therapy
- RAS and downstream RAF-MEK and PI3K-AKT signaling in neuronal development, function and dysfunction
- Defective actin dynamics in dendritic spines: cause or consequence of age-induced cognitive decline?
- Review
- Role of chitinase-like proteins in cancer
- Research Articles/Short Communications
- Cell Biology and Signaling
- Ectopic overexpression of Nanog induces tumorigenesis in non-tumorous fibroblasts
- Chemopreventive and hepatoprotective roles of adiponectin (SULF2 inhibitor) in hepatocelluar carcinoma
- Molecular Medicine
- Increased secretory sphingomyelinase activity in the first trimester of pregnancy in women later developing preeclampsia: a nested case-control study
Artikel in diesem Heft
- Frontmatter
- Guest Editorial
- Highlight: Perspectives of molecular neuroscience in health and disease
- HIGHLIGHT: CURRENT CONCE PTS OF PROTECTION AND REGE NERATION IN BRAIN DISORDERS
- The cytoskeleton as a drug target for neuroprotection: the case of the autism- mutated ADNP
- Protein aggregate formation in oligodendrocytes: tau and the cytoskeleton at the intersection of neuroprotection and neurodegeneration
- How to build the fastest receptor on earth
- Signaling pathways regulating Homer1a expression: implications for antidepressant therapy
- RAS and downstream RAF-MEK and PI3K-AKT signaling in neuronal development, function and dysfunction
- Defective actin dynamics in dendritic spines: cause or consequence of age-induced cognitive decline?
- Review
- Role of chitinase-like proteins in cancer
- Research Articles/Short Communications
- Cell Biology and Signaling
- Ectopic overexpression of Nanog induces tumorigenesis in non-tumorous fibroblasts
- Chemopreventive and hepatoprotective roles of adiponectin (SULF2 inhibitor) in hepatocelluar carcinoma
- Molecular Medicine
- Increased secretory sphingomyelinase activity in the first trimester of pregnancy in women later developing preeclampsia: a nested case-control study