ArticleMolecular biology reports2013
Overexpression of APRIN inhibits differentiation and proliferation and promotes apoptosis in P19 embryonal carcinoma cells.
Article in Molecular biology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Identification and validation of liquid biopsy-based methylation biomarkers for germ cell tumor subtypes.Communications medicine · 2026Article
- Downregulation of APRIN expression increases cancer cell proliferation via an interleukin-6/STAT3/cyclin D axis.Oncology letters · 2021Article
- miR-223 Regulates Cell Proliferation and Invasion via Targeting PDS5B in Pancreatic Cancer Cells.Molecular therapy. Nucleic acids · 2019Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously demonstrated that androgen-induced proliferation inhibitor (APRIN) expression was upregulated in ventricular septum tissues from patients with ventricular septal defect (VSD). The present study was designed to investigate the effects of APRIN on P19 cell differentiation, proliferation and apoptosis. In this study, we established a stable APRIN-overexpressing P19 embryonal carcinoma cell line that can differentiate into myocardial cells when treated with 1 % dimethyl sulfoxide. Our data showed that mRNA expressions of myocardial cell differentiation-related genes (such as cTnT, α-MHC, GATA4, and MEF2C) in the APRIN-overexpressing P19 cells were downregulated compared to the empty-vector controls. Our findings also indicated that P19 cells overexpressing APRIN had a reduced growth rate and a decreased S phase of the cell cycle. Moreover, the apoptotic rate in P19 cells overexpressing APRIN was significantly higher than that in the controls. In conclusion, our study demonstrates that overexpression of APRIN inhibits differentiation and proliferation and promotes apoptosis in P19 cells, suggesting that APRIN may be involved in the pathogenesis of VSD.
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