ArticleCellular oncology (Dordrecht, Netherlands)2017
Dual treatment with shikonin and temozolomide reduces glioblastoma tumor growth, migration and glial-to-mesenchymal transition.
Article in Cellular oncology (Dordrecht, Netherlands), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Centratherin Exhibits Antitumor Activity Against Glioblastoma Cells.Neurochemical research · 2026Article
- The multifaceted therapeutical role of low-density lipoprotein receptor family in high-grade glioma.Molecular oncology · 2024Review
- Long noncoding RNA UNC5B-AS1 suppresses cell proliferation by sponging miR-24-3p in glioblastoma multiforme.BMC medical genomics · 2024Article
- FOXO1-miR-506 axis promotes chemosensitivity to temozolomide and suppresses invasiveness in glioblastoma through a feedback loop of FOXO1/miR-506/ETS1/FOXO1.Journal of Zhejiang University. Science. B · 2023Article
- Article
- In Vitro Cytotoxic Effects and Mechanisms of Action of Eleutherine Isolated fromMolecules (Basel, Switzerland) · 2022Article
- P2X7 receptor: the regulator of glioma tumor development and survival.Purinergic signalling · 2022Article
- Overcoming therapeutic resistance to platinum-based drugs by targeting Epithelial-Mesenchymal transition.Frontiers in oncology · 2022Review
- C3G Protein, a New Player in Glioblastoma.International journal of molecular sciences · 2021Review
- Review
- Therapeutic candidates for keloid scars identified by qualitative review of scratch assay research for wound healing.PloS one · 2021Review
- High Adenosine Extracellular Levels Induce Glioblastoma Aggressive Traits Modulating the Mesenchymal Stromal Cell Secretome.International journal of molecular sciences · 2020Article
- BRCA1-associated protein inhibits glioma cell proliferation and migration and glioma stem cell self-renewal via the TGF-β/PI3K/AKT/mTOR signalling pathway.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Integrin Signaling in Glioma Pathogenesis: From Biology to Therapy.International journal of molecular sciences · 2020Review
- Inhibition of the STAT3 Signaling Pathway Contributes to the Anti-Melanoma Activities of Shikonin.Frontiers in pharmacology · 2020Article
- Human bone marrow-derived mesenchymal stem cell-secreted exosomes overexpressing microRNA-34a ameliorate glioblastoma development via down-regulating MYCN.Cellular oncology (Dordrecht, Netherlands) · 2019Article
- QKI deficiency maintains glioma stem cell stemness by activating the SHH/GLI1 signaling pathway.Cellular oncology (Dordrecht, Netherlands) · 2019Article
- The tumor suppressor FOXO3a mediates the response to EGFR inhibition in glioblastoma cells.Cellular oncology (Dordrecht, Netherlands) · 2019Article
- The role of caveolin-1 in tumors of the brain - functional and clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2019Review
- A HIF-independent, CD133-mediated mechanism of cisplatin resistance in glioblastoma cells.Cellular oncology (Dordrecht, Netherlands) · 2018Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeGlioblastomas (GBM) comprise 17% of all primary brain tumors. These tumors are extremely aggressive due to their infiltrative capacity and chemoresistance, with glial-to-mesenchymal transition (GMT) proteins playing a prominent role in tumor invasion. One compound that has recently been used to reduce the expression of these proteins is shikonin (SHK), a naphthoquinone with anti-tumor properties. Temozolomide (TMZ), the most commonly used chemotherapeutic agent in GBM treatment, has so far not been studied in combination with SHK. Here, we investigated the combined effects of these two drugs on the proliferation and motility of GBM-derived cells.
methodsThe cytotoxic and proliferative effects of SHK and TMZ on human GBM-derived cells were tested using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), Ki67 staining and BrdU incorporation assays. The migration capacities of these cells were evaluated using a scratch wound assay. The expression levels of β3 integrin, metalloproteinases (MMPs) and GMT-associated proteins were determined by Western blotting and immunocytochemistry.
resultsWe found that GBM-derived cells treated with a combination of SHK and TMZ showed decreases in their proliferation and migration capacities. These decreases were followed by the suppression of GMT through a reduction of β3 integrin, MMP-2, MMP-9, Slug and vimentin expression via inactivation of PI3K/AKT signaling.
conclusionFrom our results we conclude that dual treatment with SHK and TMZ may constitute a powerful new tool for GBM treatment by reducing therapy resistance and tumor recurrence.
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