ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2015
[Mechanism of Killing Effect of Thioridazine on Human Lung Cancer PC9 Cells].
Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Phenothiazine Derivatives and Their Impact on the Apoptosis Processes: A Review.Journal of applied toxicology : JAT · 2026Review
- Repurposing Antipsychotics for Cancer Treatment.Biomedicines · 2021Review
- [Thioridazine Sensitizes Apoptotic Effect of TRAIL in Human Lung Cancer PC9 Cells Through ER Stress Mediated Up-regulation of DR5].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2017Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent research shows thioridazine which is a kind of phenothiazine antipsychotic drugs can inhibit the proliferation of various tumor cells in vitro, but the role of thioridazine on lung cancer has not been reported. So we choose PC9 cell lines as the research object, the aim is to oberve the killing effect of thioridazine on PC9 cells and investigate its possible mechanism.
methodsAfter being treated with different concentrations of thioridazine, the proliferation of PC9 cells was determined by methyl thiazolyltetrazolium (MTT) assay. Flow cytometry was used to measure the cell cycle distribution and apoptosis. The expressions of cell cycle-associated protein CyclinD1 and apoptosis-related proteins Caspase-3, Caspase-8, Caspase-9, Bcl-2, Bax and Bcl-xl were detected by Western blot.
resultsThe proliferation of PC9 cells was significantly inhibited by thioridazine in a dose- and time-dependent manner. Flow cytometry showed that cell cycle was arrested in G0/G1 phase and the apoptotic rates were significantly increased with the increasing concentration of thioridazine. Compared with the control group, the differences were statistically significant (P<0.05). Western blot analysis showed that, compared with the control group, thioridazine reduced the expressions of CyclinD1, Bcl-2 and Bcl-xl (P<0.01) and increased the expression of Bax (P<0.01). In the mean time, thioridazine promoted the activities of Caspase-3, Caspase-8 and Caspase-9 (P<0.01).
conclusionsThe mechanism of thioridazine inhibiting the proliferation of PC9 cells may be related to stimulation of Caspase apoptotic pathway, down-regulation of CyclinD1, Bcl-2, Bcl-xl and up-regulation of Bax.
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