ArticleOncogene2006
Antitumor effect of E1A in ovarian cancer by cytoplasmic sequestration of activated ERK by PEA15.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Mechanistic Insights and Clinical Implications of ELK1 in Solid Tumors: A Narrative Review.Cells · 2025Review
- A Novel Six Autophagy-Related Genes Signature Associated With Outcomes and Immune Microenvironment in Lower-Grade Glioma.Frontiers in genetics · 2021Article
- Cytoplasmic VDR expression as an independent risk factor for ovarian cancer.Histochemistry and cell biology · 2020Article
- Article
- Differential Activation of ERK Signaling in HPV-Related Oropharyngeal Squamous Cell Carcinoma.Cancers · 2019Article
- SPARCL1 suppresses the proliferation and migration of human ovarian cancer cells via the MEK/ERK signaling.Experimental and therapeutic medicine · 2018Article
- Chaperone-mediated autophagy substrate proteins in cancer.Oncotarget · 2017Review
- MKP1 mediates chemosensitizer effects of E1a in response to cisplatin in non-small cell lung carcinoma cells.Oncotarget · 2015Article
- On the Quest of Cellular Functions of PEA-15 and the Therapeutic Opportunities.Pharmaceuticals (Basel, Switzerland) · 2015Review
- Development of PEA-15 using a potent non-viral vector for therapeutic application in breast cancer.Cancer letters · 2015Article
- Linking signaling pathways to transcriptional programs in breast cancer.Genome research · 2014Article
- Phosphoprotein enriched in astrocytes (PEA)-15: a potential therapeutic target in multiple disease states.Pharmacology & therapeutics · 2014Review
- PEA15 impairs cell migration and correlates with clinical features predicting good prognosis in neuroblastoma.International journal of cancer · 2012Article
- PEA-15 unphosphorylated at both serine 104 and serine 116 inhibits ovarian cancer cell tumorigenicity and progression through blocking β-catenin.Oncogenesis · 2012Article
- MEK1/2 inhibitor selumetinib (AZD6244) inhibits growth of ovarian clear cell carcinoma in a PEA-15-dependent manner in a mouse xenograft model.Molecular cancer therapeutics · 2012Article
- High ERK protein expression levels correlate with shorter survival in triple-negative breast cancer patients.The oncologist · 2012Article
- Characterization of a MAPK scaffolding protein logic gate in gonadotropes.Molecular endocrinology (Baltimore, Md.) · 2011Article
- The PEA-15 protein regulates autophagy via activation of JNK.The Journal of biological chemistry · 2010Article
- Article
- PEA-15 induces autophagy in human ovarian cancer cells and is associated with prolonged overall survival.Cancer research · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The adenovirus type 5 gene E1A is known to suppress tumorigenicity by transcriptionally downregulating HER-2/neu (HER2) or by inducing apoptosis. We show here that E1A also suppressed the tumorigenicity of the low-HER2-expressing ovarian cancer cell line OVCAR-3 by decreasing cell proliferation. We further found that the mechanism responsible for this reduced proliferation is the presence of PEA15 (phosphoprotein enriched in astrocytes), which is upregulated by E1A in ovarian cancer; PEA15 promotes translocation of ERK from the nucleus to the cytoplasm, leading to inhibition of ERK-dependent transcription and proliferation. Indeed, siRNA-mediated knockdown of PEA15 expression in OVCAR-3 stable E1A transfectants resulted in a nuclear accumulation of the active form of ERK, followed by an increase in Elk-1 activity, DNA synthesis, and anchorage-independent growth. Finally, PEA15 by itself suppressed colony formation in breast and ovarian cancer cell lines, in which E1A is known to have antitumor activity. We conclude that part of the antitumor effect of E1A in ovarian cancer results from cytoplasmic sequestration of the activated form of ERK by PEA15.
Indexed as
Identifiers
What OpenQuestion holds
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.