ArticleJournal of Cancer2014
Preferential effect of akt2-dependent signaling on the cellular viability of ovarian cancer cells in response to EGF.
Article in Journal of Cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Integrated multi-dimensional comparison of proteomic profiles across 54 cancer cell lines.iScience · 2025Article
- Stereochemical engineering yields a multifunctional peptide macrocycle inhibitor of Akt2 by fine-tuning macrocycle-cell membrane interactions.Communications chemistry · 2023Article
- Integrative microRNA and gene expression analysis identifies new epigenetically regulated microRNAs mediating taxane resistance in ovarian cancer.Scientific reports · 2021Article
- Multi-kinase targeted therapy as a promising treatment strategy for ovarian tumors expressing sfRon receptor.Genes & cancer · 2020Article
- Ovarian Cells Have Increased Proliferation in Response to Heparin-Binding Epidermal Growth Factor as Collagen Density Increases.Tissue engineering. Part A · 2020Article
- CXCR2 is a negative regulator of p21 in p53-dependent and independent manner via Akt-mediated Mdm2 in ovarian cancer.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveOverexpression of the epidermal growth factor receptor (EGFR) is associated with the malignant phenotype in many cancers including ovarian cancer, which leads to increased cell proliferation and survival. In spite of emerging EGFR inhibitors as a potentially useful agent, they are largely ineffective in patients with advanced or recurrent ovarian cancers. Since Akt as a key downstream factor of EGFR is highly activated in some high grade serous ovarian tumors, the augmented Akt activation may attribute to irregular EGFR-mediated signaling observed in ovarian cancer. Here we investigated the differential effect of Akt on the EGF-induced cell viability in a panel of ovarian cancer cell lines.
methodsCellular viability assay and western blot analysis were used to measure cell viability and expression levels of proteins, respectively. Knockdown of Akt was achieved with siRNA and stable transfection of expression vectors was performed.
resultsCellular viability increased in OVCAR-3 ovarian cancer cells exposed to EGF, but little to no difference was observed in the 5 other ovarian cancer cells including SKOV-3 cells despite of the expression of EGFR. In OVCAR-3 cells, EGF activated Erk and Akt, but an Erk inhibitor had no impact on cellular viability. On the other hand, the EGFR and PI3K inhibitors decreased EGF-induced cellular viability, indicating the involvement of Akt signaling. Although EGF activated Erk in SKOV-3 cells, the Akt activation was very weak as compared to OVCAR-3 cells. Furthermore, we observed a different expression of Akt isoforms: Akt1 was constitutively expressed in all tested ovarian cancer cells, while Akt3 was little expressed. Interestingly, Akt2 was highly expressed in OVCAR-3 cells. Knockdown of Akt2 blocked EGF-induced OVCAR-3 cell viability whereas knockdown for Akt1 and Erk1/2 had no significant effect. Stable transfection of Akt2 into SKOV-3 cells phosphorylated more Akt and enhanced cell viability in response to EGF.
conclusionsAkt2-dependent signaling appears to play an important role in EGFR-mediated cellular viability in ovarian cancer and targeting specific Akt isoform may provide a potential therapeutic approach for EGFR-expressing ovarian cancers.
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