ArticleCell death & disease2018
Endogenous authentic OCT4A proteins directly regulate FOS/AP-1 transcription in somatic cancer cells.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 25 citations in OpenAlex.
- Multifaceted role ofiScience · 2026Article
- Multifaceted roles of OCT4 in tumor microenvironment: biology and therapeutic implications.Oncogene · 2025Review
- OCT4 translationally promotes AKT signaling as an RNA-binding protein in stressed pluripotent stem cells.Stem cell research & therapy · 2025Article
- Proteomics Can Rise to the Challenge of Pseudogenes' Coding Nature.Journal of proteome research · 2024Review
- Article
- Use of High-Plex Data Reveals Novel Insights into the Tumour Microenvironment of Clear Cell Renal Cell Carcinoma.Cancers · 2022Article
- Endothelial OCT4 is atheroprotective by preventing metabolic and phenotypic dysfunction.Cardiovascular research · 2022Article
- The Concept of "Cancer Stem Cells" in the Context of Classic Carcinogenesis Hypotheses and Experimental Findings.Life (Basel, Switzerland) · 2021Article
- In Search of a Unifying Concept in Human Diseases.Diseases (Basel, Switzerland) · 2021Article
- Article
- Gene Editing in Pluripotent Stem Cells and Their Derived Organoids.Stem cells international · 2021Review
- Combined inhibition of JAK1/2 and DNMT1 by newly identified small-molecule compounds synergistically suppresses the survival and proliferation of cervical cancer cells.Cell death & disease · 2020Article
- Prognostic value of OCT4A and SPP1C transcript variant co-expression in early-stage lung adenocarcinoma.BMC cancer · 2020Article
- Multiple novel hepatocellular carcinoma signature genes are commonly controlled by the master pluripotency factor OCT4.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Role of Oct3/4 in Cervical Cancer Tumorigenesis.Frontiers in oncology · 2020Review
- Systematic expression alteration analysis of master reprogramming factor OCT4 and its three pseudogenes in human cancer and their prognostic outcomes.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
Abstract
OCT4A is well established as a master transcription factor for pluripotent stem cell (PSC) self-renewal and a pioneer factor for initiating somatic cell reprogramming, yet its presence and functionality in somatic cancer cells remain controversial and obscure. By combining the CRISPR-Cas9-based gene editing with highly specific PCR assays, highly sensitive immunoassays, and mass spectrometry, we provide unequivocal evidence here that full-length authentic OCT4A transcripts and proteins were both present in somatic cancer cells, and OCT4A proteins were heterogeneously expressed in the whole cell population and when expressed, they are predominantly localized in cell nucleus. Despite their extremely low abundance (approximately three orders of magnitude lower than in PSCs), OCT4A proteins bound to the promoter/enhancer regions of the AP-1 transcription factor subunit c-FOS gene and critically regulated its transcription. Knocking out OCT4A in somatic cancer cells led to dramatic reduction of the c-FOS protein level, aberrant AP-1 signaling, dampened self-renewal capacity, deficient cell migration that were associated with cell growth retardation in vitro and in vivo, and their enhanced sensitivity to anticancer drugs. Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic 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.