ArticleThe Journal of biological chemistry2018
Thioridazine inhibits self-renewal in breast cancer cells via DRD2-dependent STAT3 inhibition, but induces a G
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- STAT3 as a potential therapeutic target in triple negative breast cancer: a systematic review.Journal of experimental & clinical cancer research : CR · 2019Pooled it
- Targeting the nervous system: Mechanistic insights into neuro-tumor communication and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- A Novel DRD2 Antagonist, SD2-2305, Exerts Anticancer Effects in Colorectal Cancer Cells through G1 Arrest and Caspase-Dependent Apoptosis.Biomolecules & therapeutics · 2026Article
- Neuroprotective Effects of Phenothiazines on Acute Ischemic Stroke.CNS neuroscience & therapeutics · 2026Review
- Repurposing Quetiapine as an Adjuvant Therapeutic Agent for Triple-Negative Breast Cancer.Radiation research · 2026Article
- Targeting STAT3 in Breast Cancer Using Innovative Natural and Synthetic Scaffolds to Trigger Apoptosis, Autophagy, and Halt Tumor Progression.Current drug targets · 2026Review
- The role of dordaviprone in the multidisciplinary management of diffuse midline glioma.Surgical neurology international · 2026Review
- Phenothiazine Derivatives and Their Impact on the Apoptosis Processes: A Review.Journal of applied toxicology : JAT · 2026Review
- Nicotinic Acetylcholine Receptor Pathways in Cancer: From Psychiatric Clues to Therapeutic Opportunities.Cancer reports (Hoboken, N.J.) · 2025Review
- Editorial: Drug repurposing for cancer treatment: current and future directions.Frontiers in oncology · 2025Article
- Steaming duration-dependent effects on theFrontiers in pharmacology · 2025Article
- Revealing New Prospects: Antipsychotic Drugs Induces Anti-tumor Effects against Gastric Cancer through Inducing Apoptosis.Current cancer drug targets · 2025Article
- Therapeutic strategies for colorectal cancer: antitumor efficacy of dopamine D2 receptor antagonists.Toxicological research · 2024Review
- A review of current therapeutics targeting the mitochondrial protease ClpP in diffuse midline glioma, H3 K27-altered.Neuro-oncology · 2024Review
- Domperidone Exerts Antitumor Activity in Triple-Negative Breast Cancer Cells by Modulating Reactive Oxygen Species and JAK/STAT3 Signaling.Biomolecules & therapeutics · 2023Article
- Article
- Review
- Dissecting the novel abilities of aripiprazole: The generation of anti-colorectal cancer effects by targeting GActa pharmaceutica Sinica. B · 2023Article
- The anti-cancer efficacy of a novel phenothiazine derivative is independent of dopamine and serotonin receptor inhibition.Frontiers in oncology · 2023Article
- Exploring neurotransmitters and their receptors for breast cancer prevention and treatment.Theranostics · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Thioridazine is an antipsychotic that has been shown to induce cell death and inhibit self-renewal in a broad spectrum of cancer cells. The mechanisms by which these effects are mediated are currently unknown but are presumed to result from the inhibition of dopamine receptor 2 (DRD2). Here we show that the self-renewal of several, but not all, triple-negative breast cancer cell lines is inhibited by thioridazine. The inhibition of self-renewal by thioridazine in these cells is mediated by DRD2 inhibition. Further, we demonstrate that DRD2 promotes self-renewal in these cells via a STAT3- and IL-6-dependent mechanism. We also show that thioridazine induces a G
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.