ArticleJournal of cellular physiology2010
Transcriptional regulation of Rex1 (zfp42) in normal prostate epithelial cells and prostate cancer cells.
Article in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- A ZFP42/MARK2 regulatory network reduces the damage of retinal ganglion cells in glaucoma: a study based on GEO dataset and in vitro experiments.Apoptosis : an international journal on programmed cell death · 2022Article
- The long and short non-coding RNAs modulating EZH2 signaling in cancer.Journal of hematology & oncology · 2022Review
- REX1 promotes EMT-induced cell metastasis by activating the JAK2/STAT3-signaling pathway by targeting SOCS1 in cervical cancer.Oncogene · 2019Article
- Review
- Upregulation of miR-146a by YY1 depletion correlates with delayed progression of prostate cancer.International journal of oncology · 2017Article
- Mechanisms Regulating Stemness and Differentiation in Embryonal Carcinoma Cells.Stem cells international · 2017Review
- Embryonic stem cell markers.Molecules (Basel, Switzerland) · 2012Review
- Rex1 (Zfp42) null mice show impaired testicular function, abnormal testis morphology, and aberrant gene expression.Developmental biology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Rex1 (zfp42) was identified by our laboratory because of its reduced expression in F9 teratocarcinoma stem cells after retinoic acid (RA) treatment. The Rex1 (Zfp42) gene is currently widely used as a marker of embryonic stem cells. We compared the transcriptional regulation of the human Rex1 gene in NTera-2 (NT-2) human teratocarcinoma, normal human prostate epithelial cells (PrEC), and prostate cancer cells (PC-3) by promoter/luciferase analyses. Oct4, Sox2, Nanog, and Dax1 transcripts are expressed at higher levels in NT-2 and PrEC cells than in PC-3 cells. Co-transfection analyses showed that YY1 and Rex1 are positive regulators of hRex1 transcription in NT-2 and PrEC cells, whereas Nanog is not. Serial deletion constructs of the hRex1 promoter were created and analyzed, by which we identified a potential negative regulatory site that is located between -1 and -0.4 kb of the hRex1 promoter. We also delineated regions of the hRex1 promoter between -0.4 kb and the TSS that, when mutated, reduced transcriptional activation; these are putative Rex1 binding sites. Mutation of a putative Rex1 binding site in electrophoretic mobility shift assays (EMSA) resulted in reduced protein binding. Taken together, our results indicate that hRex1 binds to the hRex1 promoter region at -298 bp and positively regulates hRex1 transcription, but that this regulation is lost in PC-3 human prostate cancer cells. This lack of positive transcriptional regulation by the hRex1 protein may be responsible for the lack of Rex1 expression in PC-3 prostate cancer cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.