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Updated: Jan 26, 2026
Activating Autophagy by Aerobic Exercise in Mice
Published on: February 3, 2017
Olanzapine induced autophagy through suppression of NF-κB activation in human glioma cells
Ying Zhu1, Yi-Fan Zhao1, Rui-Si Liu1
1Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Aims:
Our laboratory previously reported that olanzapine treatment inhibited growth of glioma cell lines and hypothesized that autophagy may be involved in the proliferation inhibitory effects of olanzapine. However, the mechanisms of olanzapine-contributed autophagy activation are unclear.
Methods:
The inhibitory effects of olanzapine on glioma cells were evaluated by CCK8 assay, Hoechst 33258 staining and annexin V-FITC/PI staining. Western blotting, nuclear separation techniques, and immunofluorescence assays were used to investigate the relationship between the inhibition of NF-κB and autophagy activation by olanzapine.
Results:
In this work, we verified that olanzapine increased autophagic flux and autophagic vesicles. In addition, we confirmed that autophagy was related to NF-κB inhibition in cancer progression, especially with the nuclear translocation of p65. Furthermore, we demonstrated that autophagy induced by olanzapine could be impaired with TNFα cotreatment. We also found that olanzapine had an inhibitory effect on T98 cells with positive MGMT protein expression, which may involve the inhibition of MGMT through effects on NF-κB.
Conclusions:
Our findings identify a pathway by which olanzapine induces autophagy by depressing NF-κB in a glioma cell line, providing evidence which supports the use of olanzapine as a potential anticancer drug.
Insights
Olanzapine inhibits glioma cell growth by activating autophagy through the suppression of NF-κB signaling. This study reveals a novel mechanism for olanzapine
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Olanzapine previously demonstrated inhibitory effects on glioma cell lines.
- Autophagy was hypothesized to mediate olanzapine's anti-proliferative effects.
- Mechanisms of olanzapine-induced autophagy remain unclear.
Purpose of the Study:
- To elucidate the mechanisms by which olanzapine activates autophagy in glioma cells.
- To investigate the role of NF-κB signaling in olanzapine-induced autophagy.
- To evaluate olanzapine as a potential anticancer therapeutic.
Main Methods:
- Cell viability assays (CCK8, Hoechst 33258, Annexin V-FITC/PI).
- Western blotting, nuclear separation, and immunofluorescence assays.
- Investigated NF-κB (p65) and autophagy markers.
Main Results:
- Olanzapine increased autophagic flux and autophagic vesicles.
- Autophagy activation correlated with NF-κB inhibition, including p65 nuclear translocation.
- Olanzapine's autophagy induction was impaired by TNFα cotreatment.
- Olanzapine inhibited T98 cells expressing MGMT, potentially via NF-κB/MGMT pathway.
Conclusions:
- Olanzapine induces autophagy by suppressing NF-κB signaling in glioma cells.
- This pathway provides mechanistic insight into olanzapine's anti-cancer effects.
- Findings support olanzapine's potential as an anticancer drug.
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