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Atorvastatin Promotes Cytotoxicity and Reduces Migration and Proliferation of Human A172 Glioma Cells
Karen A Oliveira1,2, Tharine Dal-Cim3, Flávia G Lopes4
1Programa de Pós-Graduação em Bioquímica, Florianópolis, Brazil.
Abstract:
Malignant gliomas have resistance mechanisms to chemotherapy that enable tumor invasiveness and aggressiveness. Alternative therapies in cancer treatment, as statins, have been suggested to decrease proliferation, inhibit cell migration, and induce cell death. The aim of this study was to evaluate the effect of atorvastatin (ATOR) on cell viability, migration, proliferation, apoptosis, and autophagy in A172 human glioma cells. Temozolomide (TMZ), a chemotherapic used to glioma treatment, was tested as a comparison to cytotoxic effects on gliomas. Cell viability was also assessed in primary culture of cortical astrocytes. ATOR treatment (0.1 to 20 μM) did not alter astrocytic viability. However, in glioma cells, ATOR showed cytotoxic effect at 10 and 20 μM concentrations. TMZ (500 μM) reduced cell viability similarly to ATOR, and drug association did not show additive effect on cell viability. ATOR, TMZ, and their association decreased cell migration. ATOR also decreased glioma cell proliferation. ATOR increased apoptosis, and TMZ association showed a potentiation effect, enhancing it. ATOR and TMZ treatment increased acidic vesicular organelle (AVO) presence in A172 cells, an indicative of autophagy. ATOR effect of reducing A172 cell viability did not alter glutamate transport and glutamine synthetase activity, but it was partially prevented through antagonism of ionotropic and metabotropic glutamate receptors. Our data shows a cytotoxic effect of ATOR on glioma cells, whereas no toxicity was observed to astrocytes. ATOR showed similar cytotoxic effect as TMZ to glioma cells, and it may be a safer drug, regarding side effect induction, than chemotherapic agents.
Insights
Atorvastatin (ATOR) demonstrates cytotoxic effects on malignant glioma cells, reducing viability and migration similarly to temozolomide (TMZ) without harming astrocytes. This suggests atorvastatin as a potentially safer alternative cancer therapy.
Area of Science:
- Neuroscience
- Oncology
- Pharmacology
Background:
- Malignant gliomas exhibit resistance to chemotherapy, driving tumor invasiveness and aggressiveness.
- Statins are explored as alternative cancer therapies, potentially inhibiting proliferation, migration, and inducing cell death.
Purpose of the Study:
- To evaluate the effects of atorvastatin (ATOR) on cell viability, migration, proliferation, apoptosis, and autophagy in A172 human glioma cells.
- To compare the cytotoxic effects of ATOR with temozolomide (TMZ), a standard glioma chemotherapeutic.
- To assess the safety of ATOR on primary cortical astrocytes.
Main Methods:
- A172 human glioma cells and primary cortical astrocytes were treated with varying concentrations of ATOR (0.1-20 μM) and TMZ (500 μM).
- Assays were performed to measure cell viability, migration, proliferation, apoptosis, and autophagy (indicated by acidic vesicular organelles).
- Glutamate transport and glutamine synthetase activity were assessed, along with the effects of glutamate receptor antagonists.
Main Results:
- ATOR exhibited a dose-dependent cytotoxic effect on A172 glioma cells at concentrations of 10 and 20 μM, while sparing astrocytes.
- ATOR and TMZ showed comparable reductions in glioma cell viability and migration; combined treatment did not enhance viability reduction but potentiated apoptosis.
- ATOR decreased glioma cell proliferation and increased autophagy; its effects on viability were partially mediated by glutamate receptors.
Conclusions:
- Atorvastatin demonstrates significant cytotoxic effects against malignant glioma cells in vitro, comparable to temozolomide.
- ATOR presents a potentially safer alternative to chemotherapy, as it lacks toxicity in astrocytes.
- ATOR influences multiple cancer hallmarks, including proliferation, migration, apoptosis, and autophagy, highlighting its therapeutic potential in glioma treatment.
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