Human ESC Self-Renewal Promoting microRNAs Induce Epithelial-Mesenchymal Transition in 2 Hepatocytes by Controlling the PTEN and TGFβ Tumor Suppressor Signaling Pathways
نویسندگان
چکیده
7 Transplant Research Program & UC Davis Institute for Regenerative Cures, University of California 8 Davis, Sacramento, California, 95817, USA. 9 Department of Biochemistry and Molecular Biology, University of Southern California, Los Angeles, 10 California, 90089, USA. 11 3Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, 12 Pennsylvania, 19104, USA. 13 Department of Internal Medicine, Division of Gastroenterology and Hepatology, University of 14 California Davis Medical Center, Sacramento, California, 95817, USA. 15 Department of Medicine and Dermatology, University of California San Francisco, 94142, USA. 16 Department of Urology, University of California Davis Medical Center, Sacramento, California, 95817, 17 USA. 18 19 20 21
منابع مشابه
Human ESC self-renewal promoting microRNAs induce epithelial-mesenchymal transition in hepatocytes by controlling the PTEN and TGFβ tumor suppressor signaling pathways.
The self-renewal capacity ascribed to embryonic stem cells (ESC) is reminiscent of cancer cell proliferation, raising speculation that a common network of genes may regulate these traits. A search for general regulators of these traits yielded a set of microRNAs for which expression is highly enriched in human ESCs and liver cancer cells (HCC) but attenuated in differentiated quiescent hepatocy...
متن کاملSignaling and Regulation Human ESC Self-renewal Promoting microRNAs Induce Epithelial–Mesenchymal Transition in Hepatocytes by Controlling the PTEN and TGFb Tumor Suppressor Signaling Pathways
The self-renewal capacity ascribed to embryonic stem cells (ESC) is reminiscent of cancer cell proliferation, raising speculation that a common network of genesmay regulate these traits. A search for general regulators of these traits yielded a set of microRNAs for which expression is highly enriched in human ESCs and liver cancer cells (HCC) but attenuated in differentiated quiescent hepatocyt...
متن کاملDirect regulation of transforming growth factor β‐induced epithelial–mesenchymal transition by the protein phosphatase activity of unphosphorylated PTEN in lung cancer cells
Transforming growth factor β (TGFβ) causes the acquisition of epithelial-mesenchymal transition (EMT). Although the tumor suppressor gene PTEN (phosphatase and tensin homologue deleted from chromosome 10) can negatively regulate many signaling pathways activated by TGFβ, hyperactivation of these signaling pathways is observed in lung cancer cells. We recently showed that PTEN might be subject t...
متن کاملJMJD1C Ensures Mouse Embryonic Stem Cell Self-Renewal and Somatic Cell Reprogramming through Controlling MicroRNA Expression
The roles of histone demethylases (HDMs) for the establishment and maintenance of pluripotency are incompletely characterized. Here, we show that JmjC-domain-containing protein 1c (JMJD1C), an H3K9 demethylase, is required for mouse embryonic stem cell (ESC) self-renewal. Depletion of Jmjd1c leads to the activation of ERK/MAPK signaling and epithelial-to-mesenchymal transition (EMT) to induce d...
متن کاملPEAK1 Acts as a Molecular Switch to Regulate Context-Dependent TGFβ Responses in Breast Cancer
Transforming Growth Factor β (TGFβ) has dual functions as both a tumor suppressor and a promoter of cancer progression within the tumor microenvironment, but the molecular mechanisms by which TGFβ signaling switches between these outcomes and the contexts in which this switch occurs remain to be fully elucidated. We previously identified PEAK1 as a new non-receptor tyrosine kinase that associat...
متن کامل