ArticleOncotarget2019
Inhibition of DUSP6 sensitizes ovarian cancer cells to chemotherapeutic agents via regulation of ERK signaling response genes.
Article in Oncotarget, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Dual-Specificity Protein Phosphatases Targeting Extracellular Signal-Regulated Kinases: Friends or Foes in the Biology of Cancer?International journal of molecular sciences · 2025Review
- Loss of Socs2 improves molecular responses to IFNα in a mouse model of myeloproliferative neoplasms driven by JAK2-V617F.Leukemia · 2025Article
- A novel prognostic biomarker DUSP6 promote the malignant progression of bladder cancer through mTOR mediated mitophagy.Frontiers in oncology · 2025Article
- DUSP1/MKP-1 represents another piece in the P2X7R intracellular signaling puzzle in cerebellar cells: our last journey with Mª Teresa along the purinergic pathways of Eden.Purinergic signalling · 2024Article
- Spatial transcriptomic interrogation of the tumour-stroma boundary in a 3D engineered model of ameloblastoma.Materials today. Bio · 2024Article
- In Vitro and In Silico Investigation of BCI Anticancer Properties and Its Potential for Chemotherapy-Combined Treatments.Cancers · 2023Article
- Expression of dual-specificity phosphatases in TGFß1-induced EMT in SKOV3 cells.Turkish journal of medical sciences · 2023Article
- Identification of common molecular signatures of SARS-CoV-2 infection and its influence on acute kidney injury and chronic kidney disease.Frontiers in immunology · 2023Article
- Targeting DUSP Activity as a Treatment for High-Grade Serous Ovarian Carcinoma.Molecular cancer therapeutics · 2022Article
- The cytotoxic action of BCI is not dependent on its stated DUSP1 or DUSP6 targets in neuroblastoma cells.FEBS open bio · 2022Article
- microRNA-211-5p predicts the progression of postmenopausal osteoporosis and attenuates osteogenesis by targeting dual specific phosphatase 6.Bioengineered · 2022Article
- BCI, an inhibitor of the DUSP1 and DUSP6 dual specificity phosphatases, enhances P2X7 receptor expression in neuroblastoma cells.Frontiers in cell and developmental biology · 2022Article
- Adaptive transcriptomic and immune infiltrate responses in the tumor immune microenvironment following neoadjuvant chemotherapy in high grade serous ovarian cancer reveal novel prognostic associations and activation of pro-tumorigenic pathways.Frontiers in immunology · 2022Article
- Playing cancer at its own game: activating mitogenic signaling as a paradoxical intervention.Molecular oncology · 2021Review
- Capicua in Human Cancer.Trends in cancer · 2021Review
- DUSP6 protects murine podocytes from high glucose‑induced inflammation and apoptosis.Molecular medicine reports · 2020Article
- Dual-specificity phosphatase (DUSP6) in human glioblastoma: epithelial-to-mesenchymal transition (EMT) involvement.BMC research notes · 2020Article
- High expression and potential synergy of human epididymis protein 4 and Annexin A8 promote progression and predict poor prognosis in epithelial ovarian cancer.American journal of translational research · 2020Article
- Overexpression of DUSP6 enhances chemotherapy-resistance of ovarian epithelial cancer by regulating the ERK signaling pathway.Journal of Cancer · 2020Article
- Dual specificity phosphatase 6 as a new therapeutic target candidate for epithelial ovarian cancer.Annals of translational medicine · 2019Article
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10 authors at 5 institutions in 1 country.
Funding
Abstract
Dual specificity phosphatase 6 (DUSP6) is a protein phosphatase that deactivates extracellular-signal-regulated kinase (ERK). Since the ovarian cancer biomarker human epididymis protein 4 (HE4) interacts with the ERK pathway, we sought to determine the relationship between DUSP6 and HE4 and elucidate DUSP6's role in epithelial ovarian cancer (EOC). Viability assays revealed a significant decrease in cell viability with pharmacological inhibition of DUSP6 using (E/Z)-BCI hydrochloride in ovarian cancer cells treated with carboplatin or paclitaxel, compared to treatment with either agent alone. Quantitative PCR was used to evaluate levels of ERK pathway response genes to BCI in combination with recombinant HE4 (rHE4), carboplatin, and paclitaxel. Expression of EGR1, a promoter of apoptosis, was higher in cells co-treated with BCI and paclitaxel or carboplatin than in cells treated with chemotherapeutic agents alone, while expression of the proto-oncogene c-JUN was decreased with co-treatment. The effect of BCI on the expression of these two genes opposed that of rHE4. Pathway focused quantitative PCR also revealed suppression of
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31164954PMC6534361W2952039847What OpenQuestion holds
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