ArticleACS omega2021
BIRB796, an Inhibitor of p38 Mitogen-Activated Protein Kinase, Inhibits Proliferation and Invasion in Glioblastoma Cells.
Article in ACS omega, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Anastasis: an unwelcome guest in cancer therapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Advances in targeting p38 MAPK for cancer therapy: insights from molecular pharmacology and medicinal chemistry.Molecular diversity · 2026Review
- CK2.1 Activates Chondrogenesis by Regulation of the p38 Mitogen-Activated Protein Kinase Pathway.Kinases and phosphatases · 2026Article
- The "yeast-drop" treatment protocol in theFrontiers in tuberculosis · 2026Article
- TGFβ1-TNFα-regulated secretion of neutrophil chemokines is independent of epithelial-mesenchymal transition in breast tumor cells.Molecular biology of the cell · 2025Article
- A Multicenter Study on the Prognostic Value of Indicators Derived From Complete Blood Count in Glioblastoma.Mediators of inflammation · 2025Article
- Targeting SMAD-Dependent Signaling: Considerations in Epithelial and Mesenchymal Solid Tumors.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Article
- Small molecule targeting of the p38/Mk2 stress signaling pathways to improve cancer treatment.BMC cancer · 2023Article
- The Importance of the Pyrazole Scaffold in the Design of Protein Kinases Inhibitors as Targeted Anticancer Therapies.Molecules (Basel, Switzerland) · 2023Review
- Curcumin analog HO-3867 triggers apoptotic pathways through activating JNK1/2 signalling in human oral squamous cell carcinoma cells.Journal of cellular and molecular medicine · 2022Article
- The functional role of p38 MAPK pathway in malignant brain tumors.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most common malignant tumor, and it is characterized by high cellular proliferation and invasion in the central nervous system of adults. Due to its high degree of heterogeneity and mortality, there is no effective therapy for GBM. In our study, we investigated the effect of the p38-MAPK signaling pathway inhibitor BIRB796 on GBM cells. Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2'-deoxyuridine (EDU) staining, and cell cycle distribution analysis were performed, and the results showed that BIRB796 decreased proliferation in U87 and U251 cells. Moreover, wound healing and invasion assays were performed, which showed that BIRB796 inhibited the migration and invasion of human GBM cells. We found that BIRB796 treatment significantly decreased the formation of the cytoskeleton and thus downregulated the movement ability of the cells, as shown by phalloidin staining and vimentin immunofluorescence staining. Real-time polymerase chain reaction showed that the mRNA levels of MMP-2, Vimentin, CyclinD1, and Snail-1 were downregulated. Consistently, the expressions of MMP-2, Vimentin, CyclinD1, and p-p38 were also decreased after BIRB796 treatment. Taken together, all our results demonstrated that BIRB796 could play an antitumor role by inhibiting the proliferation and invasion in GBM cells. Thus, BIRB796 may be used as an adjuvant therapy to improve the therapeutic efficacy of GBM treatment.
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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.