ArticleOncoTargets and therapy2014
Clinicopathological and biological significance of aberrant activation of glycogen synthase kinase-3 in ovarian cancer.
Article in OncoTargets and therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 18 citations in OpenAlex.
- Concurrent targeting of GSK3 and MEK as a therapeutic strategy to treat pancreatic ductal adenocarcinoma.Cancer science · 2024Article
- The many faceted role of glycogen synthase kinase-3 (GSK-3) in T cells and cancer immunotherapy.Journal of cancer biology · 2024Article
- GSK-3β Allosteric Inhibition: A Dead End or a New Pharmacological Frontier?International journal of molecular sciences · 2023Review
- Article
- 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
- Bipolar Disorder Treatments and Ovarian Cancer: A Systematic Review.Clinical neuropsychiatry · 2020Article
- Down-regulation and clinical significance of miR-7-2-3p in papillary thyroid carcinoma with multiple detecting methods.IET systems biology · 2019Article
- A nuclear shift of GSK3β protein is an independent prognostic factor in prostate cancer.Oncotarget · 2019Article
- ShenLingLan Influences the Attachment and Migration of Ovarian Cancer Cells Potentially through the GSK3 Pathway.Medicines (Basel, Switzerland) · 2017Article
- Glycogen Synthase Kinase 3 (GSK-3)-mediated Phosphorylation of Uracil N-Glycosylase 2 (UNG2) Facilitates the Repair of Floxuridine-induced DNA Lesions and Promotes Cell Survival.The Journal of biological chemistry · 2016Article
- ST6Gal-I overexpression facilitates prostate cancer progression via the PI3K/Akt/GSK-3β/β-catenin signaling pathway.Oncotarget · 2016Article
- Discrete functions of GSK3α and GSK3β isoforms in prostate tumor growth and micrometastasis.Oncotarget · 2015Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlycogen synthase kinase-3 (GSK-3) plays an important role in human cancer. The aim of this study is to evaluate the clinicopathological significance of expression of GSK-3α/β and pGSK-3α/β(Tyr279/216) in patients with epithelial ovarian cancer and to investigate whether GSK-3 inhibition can influence cell viability and tumor growth of ovarian cancer.
methodsImmunohistochemistry was used to examine expression of GSK-3α/β and pGSK-3α/β(Tyr279/216) in 71 human epithelial ovarian cancer tissues and correlations between protein expression, and clinicopathological factors were analyzed. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay following exposure of ovarian carcinoma cells to pharmacological inhibitors of GSK-3 or GSK-3 small interfering RNA. In vivo validation of tumor growth inhibition was performed with xenograft mice.
resultsThe expression levels of GSK-3α/β and pGSK-3α/β(Tyr279/216) in ovarian cancers were significantly higher than those in benign tumors. High expression of GSK-3α/β was more likely to be found in patients with advanced International Federation of Gynecology and Obstetrics (FIGO) stages and high serum cancer antigen 125. Higher expression of pGSK-3α/β(Tyr279/216) was associated with advanced FIGO stages, residual tumor mass, high serum cancer antigen 125, and poor chemoresponse. Worse overall survival was revealed by Kaplan-Meier survival curves in patients with high expression of GSK-3α/β or pGSK-3α/β(Tyr279/216). Multivariate analysis indicated that FIGO stage, GSK-3α/β expression, and pGSK-3α/β(Tyr279/216) expression were independent prognostic factors for overall survival. GSK-3 inhibition by lithium chloride, 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8), or GSK-3 small interfering RNA can decrease viability of SKOV3 and SKOV3-TR30 ovarian cancer cells. Additionally, lithium chloride-treated SKOV3 xenograft mice had a significant reduction in tumor growth compared with control-treated animals.
conclusionOur findings suggest that overexpression and aberrant activation of GSK-3 may contribute to progression and poor prognosis in ovarian cancer. Inhibition of GSK-3 may be a potential therapy for ovarian cancer.
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.