ArticleScientific reports2017
EpCAM Intracellular Domain Promotes Porcine Cell Reprogramming by Upregulation of Pluripotent Gene Expression via Beta-catenin Signaling.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- SARS-CoV-2 drives upregulation of EpCAM in respiratory epithelial cells with hypercellular profile during severe COVID-19.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- EpCAM supports exit from pluripotency of embryonic stem cells via Eomes.Cell death & disease · 2026Article
- Intracellular domain of epithelial cell adhesion molecule induces Wnt receptor transcription to promote colorectal cancer progression.Journal of biomedical science · 2024Article
- Immune evasion in lung metastasis of leiomyosarcoma: upregulation of EPCAM inhibits CD8British journal of cancer · 2024Article
- The progress of induced pluripotent stem cells derived from pigs: a mini review of recent advances.Frontiers in cell and developmental biology · 2024Review
- The strategies to cure cancer patients by eradicating cancer stem-like cells.Molecular cancer · 2023Review
- Self-transfecting GMO-PMO chimera targetingMolecular therapy. Nucleic acids · 2023Article
- miRNA-mediated control of exogenousMolecular therapy. Methods & clinical development · 2022Article
- Destabilization of EpCAM dimer is associated with increased susceptibility towards cleavage by TACE.PeerJ · 2021Article
- Expression and function of epithelial cell adhesion molecule EpCAM: where are we after 40 years?Cancer metastasis reviews · 2020Review
- Membrane-associated epithelial cell adhesion molecule is slowly cleaved by γ-secretase prior to efficient proteasomal degradation of its intracellular domain.The Journal of biological chemistry · 2019Article
- Molecular network of miR-1343 regulates the pluripotency of porcine pluripotent stem cells via repressing OTX2 expression.RNA biology · 2019Article
- Preserving self-renewal of porcine pluripotent stem cells in serum-free 3i culture condition and independent of LIF and b-FGF cytokines.Cell death discovery · 2018Article
- Functions of EpCAM in physiological processes and diseases (Review).International journal of molecular medicine · 2018Review
- Spatiotemporal patterning of EpCAM is important for murine embryonic endo- and mesodermal differentiation.Scientific reports · 2018Article
- Common microRNA-mRNA interactions exist among distinct porcine iPSC lines independent of their metastable pluripotent states.Cell death & disease · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous study showed that expression of epithelial cell adhesion molecule (EpCAM) was significantly upregulated in porcine induced pluripotent stem cells (piPSCs). However, the regulatory mechanism and the downstream target genes of EpCAM were not well investigated. In this study, we found that EpCAM was undetectable in fibroblasts, but highly expressed in piPSCs. Promoter of EpCAM was upregulated by zygotic activated factors LIN28, and ESRRB, but repressed by maternal factors OCT4 and SOX2. Knocking down EpCAM by shRNA significantly reduced the pluripotent gene expression. Conversely, overexpression of EpCAM significantly increased the number of alkaline phosphatase positive colonies and elevated the expression of endogenous pluripotent genes. As a key surface-to-nucleus factor, EpCAM releases its intercellular domain (EpICD) by a two-step proteolytic processing sequentially. Blocking the proteolytic processing by inhibitors TAPI-1 and DAPT could reduce the intracellular level of EpICD and lower expressions of OCT4, SOX2, LIN28, and ESRRB. We noticed that increasing intracellular EpICD only was unable to improve activity of EpCAM targeted genes, but by blocking GSK-3 signaling and stabilizing beta-catenin signaling, EpICD could then significantly stimulate the promoter activity. These results showed that EpCAM intracellular domain required beta-catenin signaling to enhance porcine cell reprogramming.
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