ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Effects of the GSK-3β inhibitor (2Z,3E)-6-bromoindirubin-3'-oxime upon ovarian cancer cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- The Fundamental Role of Oxime and Oxime Ether Moieties in Improving the Physicochemical and Anticancer Properties of Structurally Diverse Scaffolds.International journal of molecular sciences · 2023Review
- 'Cloudbuster': a Python-based open source application for three-dimensional reconstruction and quantification of stacked biological imaging samples.Interface focus · 2022Article
- 6-Bromoindirubin-3'-Oxime Regulates Colony Formation, Apoptosis, and Odonto/Osteogenic Differentiation in Human Dental Pulp Stem Cells.International journal of molecular sciences · 2022Article
- Adenosine Receptor A2B Negatively Regulates Cell Migration in Ovarian Carcinoma Cells.International journal of molecular sciences · 2022Article
- Expression and Functional Study ofFrontiers in plant science · 2022Article
- The role of glycogen synthase kinase 3 (GSK3) in cancer with emphasis on ovarian cancer development and progression: A comprehensive review.Bosnian journal of basic medical sciences · 2021Review
- Indirubin suppresses ovarian cancer cell viabilities through the STAT3 signaling pathway.Drug design, development and therapy · 2018Article
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2 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Ovarian cancer (OC) is a deadly disease, and despite improvements in treatment, overall 5-year survival is low. Glycogen synthase kinase (GSK)-3β is a multifunctional serine/threonine kinase. We wished to ascertain if the GSK-3β inhibitor (2Z,3E)-6-bromoindirubin-3'-oxime, known as "BIO," can suppress OC development. The OC cell lines A2780 and OVCAR3 were exposed to BIO. At different time points, cell proliferation, apoptosis, cell cycle, and cell invasion/cell migration assays were carried out. Phalloidin staining was undertaken to observe lamellipodia formation. Real-time reverse transcription-polymerase chain reaction and western blotting were used to assess expression of messenger RNA (mRNA) and protein of GSK-3β, cyclin D1, matrix metalloproteinase (MMP)-9, and p21. BIO suppressed the proliferation, invasion, and migration of OC cells; reduced lamellipodia formation; and induced G1 arrest of the cell cycle. BIO exposure led to a significant downregulation of mRNA and protein expression of cyclin D1 and MMP9 in comparison with untreated control cells. In contrast, BIO exposure upregulated mRNA and protein expression of p21 in comparison with untreated control cells. Besides, GSK-3β small interfering RNA (siRNA) transfection in ovarian cancer cells also downregulated GSK-3β, cyclin D1, and MMP9 protein expression while upregulated p21 expression. These data suggest that BIO, as an inhibitor of GSK-3β, can suppress OC development. Therefore, BIO could be a candidate drug for the treatment of OC.
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