ArticleActa pharmacologica Sinica2012
Anisomycin induces glioma cell death via down-regulation of PP2A catalytic subunit in vitro.
Article in Acta pharmacologica Sinica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Hesperetin but not ellagic acid increases myosin heavy chain expression and cell fusion in C2C12 myoblasts in the presence of oxidative stress.Frontiers in nutrition · 2024Article
- Comprehensive investigation of the prognostic values and molecular mechanisms of syntaxin binding protein 5 antisense RNA 1 in patients with colon adenocarcinoma based on RNA sequencing dataset.Journal of Cancer · 2023Article
- Anisomycin has the potential to induce human ovarian cancer stem cell ferroptosis by influencing glutathione metabolism and autophagy signal transduction pathways.Journal of Cancer · 2023Article
- Review
- GNG12 as A Novel Molecular Marker for the Diagnosis and Treatment of Glioma.Frontiers in oncology · 2022Article
- Anisomycin has a potential toxicity of promoting cuproptosis in human ovarian cancer stem cells by attenuating YY1/lipoic acid pathway activation.Journal of Cancer · 2022Article
- Rational Design, Optimization, and Biological Evaluation of Novel MEK4 Inhibitors against Pancreatic Adenocarcinoma.ACS medicinal chemistry letters · 2021Article
- Identification and validation of RNA-binding protein-related gene signature revealed potential associations with immunosuppression and drug sensitivity in glioma.Cancer medicine · 2021Article
- The mutual regulatory loop between TPTEP1 and miR-1303 in leukemogenesis of acute myeloid leukemia.Cancer cell international · 2021Article
- Expression level of long non-coding RNA colon adenocarcinoma hypermethylated serves as a novel prognostic biomarker in patients with thyroid carcinoma.Bioscience reports · 2021Article
- The Prognostic Significance of Anisomycin-Activated Phospho-c-Jun NH2-Terminal Kinase (p-JNK) in Predicting Breast Cancer Patients' Survival Time.Frontiers in cell and developmental biology · 2021Article
- Integrative Analysis of a Novel Eleven-Small Nucleolar RNA Prognostic Signature in Patients With Lower Grade Glioma.Frontiers in oncology · 2021Article
- FGF20 Protected Against BBB Disruption After Traumatic Brain Injury by Upregulating Junction Protein Expression and Inhibiting the Inflammatory Response.Frontiers in pharmacology · 2020Article
- Identification of a Metabolism-Related Risk Signature Associated With Clinical Prognosis in Glioblastoma Using Integrated Bioinformatic Analysis.Frontiers in oncology · 2020Article
- Combinatorial targeting of MTHFD2 and PAICS in purine synthesis as a novel therapeutic strategy.Cell death & disease · 2019Article
- Review
- microRNA let-7c is essential for the anisomycin-elicited apoptosis in Jurkat T cells by linking JNK1/2 to AP-1/STAT1/STAT3 signaling.Scientific reports · 2016Article
- Nuclear Protein Phosphatase 1 α (PP1A) Expression is Associated with Poor Prognosis in p53 Expressing Glioblastomas.Pathology oncology research : POR · 2016Article
- Development of a high-content screen for the identification of inhibitors directed against the early steps of the cytomegalovirus infectious cycle.Antiviral research · 2015Article
- Phosphorylation of AKT induced by phosphorylated Hsp27 confers the apoptosis-resistance in t-AUCB-treated glioblastoma cells in vitro.Journal of neuro-oncology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo examine the effects of anisomycin on glioma cells and the related mechanisms in vitro.
methodsThe U251 and U87 human glioblastoma cell lines were tested. The growth of the cells was analyzed using a CCK-8 cell viability assay. Apoptosis was detected using a flow cytometry assay. The expression of proteins and phosphorylated kinases was detected using Western blotting.
resultsTreatment of U251 and U87 cells with anisomycin (0.01-8 μmol/L) inhibited the cell growth in time- and concentration-dependent manners (the IC(50) values at 48 h were 0.233±0.021 and 0.192±0.018 μmol/L, respectively). Anisomycin (4 μmol/L) caused 21.5%±2.2% and 25.3%±3.1% of apoptosis proportion, respectively, in U251 and U87 cells. In the two cell lines, anisomycin (4 μmol/L) activated p38 MAPK and JNK, and inactivated ERK1/2. However, neither the p38 MAPK inhibitor SB203580 (10 μmol/L) nor the JNK inhibitor SP600125 (10 μmol/L) prevented anisomycin-induced cell death. On the other hand, anisomycin (4 μmol/L) reduced the level of PP2A/C subunit (catalytic subunit) in a time-dependent manner in the two cell lines. Treatment of the two cell lines with the PP2A inhibitor okadaic acid (100 nmol/L) caused marked cell death.
conclusionAnisomycin induces glioma cell death via down-regulation of PP2A catalytic subunit. The regulation of PP2A/C exression by anisomycin provides a clue to further study on its role in glioma therapy.
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