ArticleOncogenesis2012
PEA-15 unphosphorylated at both serine 104 and serine 116 inhibits ovarian cancer cell tumorigenicity and progression through blocking β-catenin.
Article in Oncogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- A system-wide investigation into the phosphoregulatory network of TNIK and its cellular implications.Frontiers in bioinformatics · 2026Article
- PEA-15 engages in allosteric interactions using a common scaffold in a phosphorylation-dependent manner.Scientific reports · 2022Article
- Proteomics analysis identifies PEA-15 as an endosomal phosphoprotein that regulates α5β1 integrin endocytosis.Scientific reports · 2021Article
- Phosphorylation of PED/PEA-15 at Ser116 and phosphorylation of p27 at Thr187 indicates a poor prognosis in hepatocellular carcinoma.Oncology letters · 2021Article
- ZNF703 promotes tumor progression in ovarian cancer by interacting with HE4 and epigenetically regulating PEA15.Journal of experimental & clinical cancer research : CR · 2020Article
- Exosomes: Insights from Retinoblastoma and Other Eye Cancers.International journal of molecular sciences · 2020Review
- Article
- The microRNA212 regulated PEA15 promotes ovarian cancer progression by inhibiting of apoptosis.Journal of Cancer · 2020Article
- PEA-15 C-Terminal Tail Allosterically Modulates Death-Effector Domain Conformation and Facilitates Protein-Protein Interactions.International journal of molecular sciences · 2019Article
- Reproducible Large-Scale Synthesis of Surface Silanized Nanoparticles as an Enabling Nanoproteomics Platform: Enrichment of the Human Heart Phosphoproteome.Nano research · 2019Article
- PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway.Oncology reports · 2019Article
- Phosphoprotein enriched in diabetes (PED/PEA15) promotes migration in hepatocellular carcinoma and confers resistance to sorafenib.Cell death & disease · 2017Article
- MEK Inhibitor Selumetinib (AZD6244; ARRY-142886) Prevents Lung Metastasis in a Triple-Negative Breast Cancer Xenograft Model.Molecular cancer therapeutics · 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
- Tissue Specific Promoters in Colorectal Cancer.Disease markers · 2015Review
- Phosphorylation-regulated degradation of the tumor-suppressor form of PED by chaperone-mediated autophagy in lung cancer cells.Journal of cellular physiology · 2014Article
- Phosphoprotein enriched in astrocytes (PEA)-15: a potential therapeutic target in multiple disease states.Pharmacology & therapeutics · 2014Review
- Bisphosphorylated PEA-15 sensitizes ovarian cancer cells to paclitaxel by impairing the microtubule-destabilizing effect of SCLIP.Molecular cancer therapeutics · 2013Article
- High Expression of PEA15 Is Associated With Patient Survival in Malignant Pleural Mesothelioma.Cancer diagnosis & prognosisArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Ovarian cancer is a major cause of death among women; there remains an urgent need to develop new effective therapies to target this cancer. Phosphoprotein enriched in astrocytes (PEA-15) is a 15-kDa phosphoprotein that is known to bind ERK1/2, thus blocking cell proliferation. The physiological activity of PEA-15 is dependent on the phosphorylation status of serine 104 (Ser104) and Ser116. However, little is known about the impact of PEA-15 phosphorylation on tumor progression. We have previously shown that overexpression of PEA-15 has an antitumor effect against both breast and ovarian cancer cells. Here, we report that using a human ovarian cancer tissue microarray, we found that tissues from patients with ovarian cancer were significantly more likely than adjacent normal tissues to express PEA-15 phosphorylated at both sites. Using phosphomimetic and nonphosphorylatable mutants of PEA-15, we found that mutant double-unphosphorylated PEA-15 in which Ser104 and Ser116 were substituted with alanine (PEA-15-AA) had a more potent antitumorigenic effect in ovarian cancer than did phosphomimetic PEA-15 in which Ser104 and Ser116 were substituted with aspartic acid (PEA-15-DD). Further, we observed that the antitumorigenic effect of PEA-15-AA was a result of inhibition of the migration capacity of cells and inhibition of in vivo angiogenesis. This inhibition was partially dependent on inhibition of β-catenin expression and nuclear translocalization. Taken together, our results suggest that phosphorylated PEA-15 is an important contributor to the aggressiveness of ovarian cancer and justify the development of PEA-15-AA as an effective therapeutic molecule in the treatment of ovarian cancer.
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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.