ArticleOncotarget2014
Glycogen synthase kinase-3β inhibition depletes the population of prostate cancer stem/progenitor-like cells and attenuates metastatic growth.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Lumbrokinase (LK) ameliorates diabetic kidney disease renal fibrosis through regulating snail via m6A RNA methyltransferase 3.Scientific reports · 2024Article
- PQR309, a dual PI3K/mTOR inhibitor, synergizes with gemcitabine by impairing the GSK-3β and STAT3/HSP60 signaling pathways to treat nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Understanding and targeting prostate cancer cell heterogeneity and plasticity.Seminars in cancer biology · 2022Review
- HGK promotes metastatic dissemination in prostate cancer.Scientific reports · 2021Article
- GSK-3β Regulates the Expression of P21 to Promote the Progression of Chordoma.Cancer management and research · 2021Article
- Review
- RETRACTED: Nitric Oxide Donor DETA/NO Inhibits the Growth of Endometrial Cancer Cells by Upregulating the Expression of RASSF1 and CDKN1A.Molecules (Basel, Switzerland) · 2019Article
- PNU-74654 enhances the antiproliferative effects of 5-FU in breast cancer and antagonizes thrombin-induced cell growth via the Wnt pathway.Journal of cellular physiology · 2019Article
- Cellular and Molecular Mechanisms Underlying Prostate Cancer Development: Therapeutic Implications.Medicines (Basel, Switzerland) · 2019Review
- Glycogen synthase kinase-3 beta inhibitors as novel cancer treatments and modulators of antitumor immune responses.Cancer biology & therapy · 2019Review
- AnFrontiers in oncology · 2018Article
- 6-bromo-indirubin-3'-oxime (6BIO), a Glycogen synthase kinase-3β inhibitor, activates cytoprotective cellular modules and suppresses cellular senescence-mediated biomolecular damage in human fibroblasts.Scientific reports · 2017Article
- CRIPTO and its signaling partner GRP78 drive the metastatic phenotype in human osteotropic prostate cancer.Oncogene · 2017Article
- Molecular Pathways: Revisiting Glycogen Synthase Kinase-3β as a Target for the Treatment of Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Review
- MiR-410 induces stemness by inhibiting Gsk3β but upregulating β-catenin in non-small cells lung cancer.Oncotarget · 2017Article
- ALK1Fc Suppresses the Human Prostate Cancer Growth inFrontiers in cell and developmental biology · 2017Article
- Prostate Cancer Stem Cells and Nanotechnology: A Focus on Wnt Signaling.Frontiers in pharmacology · 2017Review
- Nestin suppression attenuates invasive potential of endometrial cancer cells by downregulating TGF-β signaling pathway.Oncotarget · 2016Article
- ST6Gal-I overexpression facilitates prostate cancer progression via the PI3K/Akt/GSK-3β/β-catenin signaling pathway.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells with stem or progenitor properties play a pivotal role in the initiation, recurrence and metastatic potential of solid tumors, including those of the human prostate. Cancer stem cells are generally more resistant to conventional therapies thus requiring the characterization of key pathways involved in the formation and/or maintenance of this malignant cellular subpopulation. To this end, we identified Glycogen Synthase Kinase-3β (GSK-3β) as a crucial kinase for the maintenance of prostate cancer stem/progenitor-like cells and pharmacologic inhibition of GSK-3β dramatically decreased the size of this cellular subpopulation. This was paralleled by impaired clonogenicity, decreased migratory potential and dramatic morphological changes. In line with our in vitro observations, treatment with a GSK-3β inhibitor leads to a complete loss of tumorigenicity and a decrease in metastatic potential in preclinical in vivo models. These observed anti-tumor effects appear to be largely Wnt-independent as simultaneous Wnt inhibition does not reverse the observed antitumor effects of GSK-3β blockage. We found that GSK-3β activity is linked to cytoskeletal protein F-actin and inhibition of GSK-3β leads to disturbance of F-actin polymerization. This may underlie the dramatic effects of GSK-3β inhibition on prostate cancer migration. Furthermore, GSK-3β inhibition led to strongly decreased expression of several integrin types including the cancer stem cell-associated α2β1 integrin. Taken together, our mechanistic observations highlight the importance of GSK-3β activity in prostate cancer stemness and may facilitate the development of novel therapy for advanced prostate cancer.
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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.