ArticleCell journal2016
Differential Expression of OCT4 Pseudogenes in Pluripotent and Tumor Cell Lines.
Article in Cell journal, 2016. 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, 31 citations in OpenAlex.
- Pseudogenes in the carcinogenesis: epithelial-to-mesenchymal transition process and cancer initiating cells.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025Review
- Pseudogene OCT4-pg5 upregulates OCT4B expression to promote bladder cancer progression by competing with miR-145-5p.Cell cycle (Georgetown, Tex.) · 2024Article
- Expression ofFrontiers in oncology · 2023Article
- Pseudogenes and Liquid Phase Separation in Epigenetic Expression.Frontiers in oncology · 2022Review
- In Silico Analysis to Explore Lineage-Independent and -Dependent Transcriptional Programs Associated with the Process of Endothelial and Neural Differentiation of Human Induced Pluripotent Stem Cells.Journal of clinical medicine · 2021Article
- An Overview on the Complexity of OCT4: at the Level of DNA, RNA and Protein.Stem cell reviews and reports · 2021Review
- Novel Variant of OCT4, Named OCT4B5, is Highly Expressed in Human Pluripotent Cells.Stem cell reviews and reports · 2021Article
- ThemicroPublication biology · 2021Article
- FUS-dependent loading of SUV39H1 to OCT4 pseudogene-lncRNA programs a silencing complex with OCT4 promoter specificity.Communications biology · 2020Article
- Human mid-trimester amniotic fluid (stem) cells lack expression of the pluripotency marker OCT4A.Scientific reports · 2019Article
- Systematic expression alteration analysis of master reprogramming factor OCT4 and its three pseudogenes in human cancer and their prognostic outcomes.Scientific reports · 2018Article
- Complementarity of assembly-first and mapping-first approaches for alternative splicing annotation and differential analysis from RNAseq data.Scientific reports · 2018Article
- New insights into long noncoding RNAs and pseudogenes in prognosis of renal cell carcinoma.Cancer cell international · 2018Article
- Primary cultures of human colon cancer as a model to study cancer stem cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- A novel Oct4/Pou5f1-like non-coding RNA controls neural maturation and mediates developmental effects of ethanol.Neurotoxicology and teratologyArticle
- A Novel Variant ofAvicenna journal of medical biotechnologyArticle
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
objectiveThe human OCT4 gene, the most important pluripotency marker, can generate at least three different transcripts (OCT4A, OCT4B, and OCT4B1) by alternative splicing. OCT4A is the main isoform responsible for the stemness property of embryonic stem (ES) cells. There also exist eight processed OCT4 pseudogenes in the human genome with high homology to the OCT4A, some of which are transcribed in various cancers. Recent conflicting reports on OCT4 expression in tumor cells and tissues emphasize the need to discriminate the expression of OCT4A from other variants as well as OCT4 pseudogenes. MATERIALS AND
methodsIn this experimental study, DNA sequencing confirmed the authenticity of transcripts of OCT4 pseudogenes and their expression patterns were investigated in a panel of different human cell lines by reverse transcription-polymerase chain reaction (RT-PCR).
resultsDifferential expression of OCT4 pseudogenes in various human cancer and pluripotent cell lines was observed. Moreover, the expression pattern of OCT4-pseudogene 3 (OCT4-pg3) followed that of OCT4A during neural differentiation of the pluripotent cell line of NTERA-2 (NT2). Although OCT4-pg3 was highly expressed in undifferentiated NT2 cells, its expression was rapidly down-regulated upon induction of neural differentiation. Analysis of protein expression of OCT4A, OCT4-pg1, OCT4-pg3, and OCT4-pg4 by Western blotting indicated that OCT4 pseudogenes cannot produce stable proteins. Consistent with a newly proposed competitive role of pseudogene microRNA docking sites, we detected miR-145 binding sites on all transcripts of OCT4 and OCT4 pseudogenes.
conclusionOur study suggests a potential coding-independent function for OCT4 pseudogenes during differentiation or tumorigenesis.
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