ArticleInternational journal of molecular sciences2021
Involvement of PI3K Pathway in Glioma Cell Resistance to Temozolomide Treatment.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Defined pulsed electro-magnetic field exposure suppresses stemness and potentiates temozolomide-induced apoptosis in glioblastoma cells.Scientific reports · 2026Article
- A prognostic gene signature derived from aging-related genes predicts survival, immune landscape and therapy response in glioma.Molecular and clinical oncology · 2026Article
- Review
- Targeting PPARα activation sensitizes glioblastoma cells to temozolomide and reverses acquired resistance by inhibiting H3K18 lactylation.Acta pharmacologica Sinica · 2025Article
- Cell-Specific Vulnerability of Human Glioblastoma and Astrocytoma Cells to Mephedrone-An In Vitro Study.Molecules (Basel, Switzerland) · 2025Article
- Adiponectin facilitates the cell cycle, inhibits cell apoptosis and induces temozolomide resistance in glioblastoma via the Akt/mTOR pathway.Oncology letters · 2025Article
- Emerging Insights into the PI3K/AKT/mTOR Signaling Pathway and Non-Coding RNA-mediated Drug Resistance in Glioblastoma.Current molecular medicine · 2025Review
- COL22A1 Activates the PI3K/AKT Signaling Pathway to Sustain the Malignancy of Glioblastoma.International journal of genomics · 2025Article
- Multifunctional nanoplatforms based on RNA interference for glioma treatment.American journal of cancer research · 2025Review
- Exploring glioma heterogeneity through omics networks: from gene network discovery to causal insights and patient stratification.BioData mining · 2024Article
- A Synopsis of Biomarkers in Glioblastoma: Past and Present.Current issues in molecular biology · 2024Review
- Furanocoumarins as Enhancers of Antitumor Potential of Sorafenib and LY294002 toward Human Glioma Cells In Vitro.International journal of molecular sciences · 2024Article
- Article
- Anti-Glioma Effects of Ligustilide or n-Butylphthalide on Their Own and the Synergistic Effects with Temozolomide via PI3K/Akt Signaling Pathway.OncoTargets and therapy · 2023Article
- Regulation of temozolomide resistance via lncRNAs: Clinical and biological properties of lncRNAs in gliomas (Review).International journal of oncology · 2022Review
- Molecular and Circulating Biomarkers in Patients with Glioblastoma.International journal of molecular sciences · 2022Review
- Advances in medical treatment for pancreatic neuroendocrine neoplasms.World journal of gastroenterology · 2022Review
- The Role of Hsp27 in Chemotherapy Resistance.Biomedicines · 2022Review
- Immune Landscape in PTEN-Related Glioma Microenvironment: A Bioinformatic Analysis.Brain sciences · 2022Article
- DFT investigation on the application of pure and doped XRoyal Society open science · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the study was to investigate the anticancer potential of LY294002 (PI3K inhibitor) and temozolomide using glioblastoma multiforme (T98G) and anaplastic astrocytoma (MOGGCCM) cells. Apoptosis, autophagy, necrosis, and granules in the cytoplasm were identified microscopically (fluorescence and electron microscopes). The mitochondrial membrane potential was studied by flow cytometry. The activity of caspases 3, 8, and 9 and Akt was evaluated fluorometrically, while the expression of Beclin 1, PI3K, Akt, mTOR, caspase 12, and Hsp27 was determined by immunoblotting. SiRNA was used to block Hsp27 and PI3K expression. Cell migration and localization of Hsp27 were tested with the wound healing assay and immunocytochemistry, respectively. LY294002 effectively diminished the migratory potential and increased programmed death of T98G and MOGGCCM. Autophagy was dominant in MOGGCCM, while apoptosis was dominant in T98G. LY294002 with temozolomide did not potentiate cell death but redirected autophagy toward apoptosis, which was correlated with ER stress. A similar effect was observed after blocking PI3K expression with siRNA. Transfection with Hsp27 siRNA significantly increased apoptosis related to ER stress. Our results indicate that inhibition of the PI3K/Akt/mTOR pathway sensitizes glioma cells to apoptosis upon temozolomide treatment, which was correlated with ER stress. Hsp27 increases the resistance of glioma cells to cell death upon temozolomide treatment.
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