ArticleOncotarget2015
Repositioning antipsychotic chlorpromazine for treating colorectal cancer by inhibiting sirtuin 1.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.
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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
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Who cites it
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.
- Drug repositioning: Progress and challenges in drug discovery for various diseases.European journal of medicinal chemistry · 2022Pooled it
- Survival and Clinicopathological Significance of SIRT1 Expression in Cancers: A Meta-Analysis.Frontiers in endocrinology · 2019Pooled it
- Understanding nerve-tumor interactions: From basic biology to therapeutic innovation.Genes & diseases · 2026Review
- Repurposing tricyclic drugs as cancer therapeutics: comparative analysis of antitumorigenic effects of chlorpromazine, amitriptyline and imipramine.Frontiers in oncology · 2026Article
- Phenothiazine Derivatives and Their Impact on the Apoptosis Processes: A Review.Journal of applied toxicology : JAT · 2026Review
- Repurposing chlorpromazine for the treatment of triple-negative breast cancer growth and metastasis based on modulation of mitochondria-mediated apoptosis and autophagy/mitophagy.British journal of cancer · 2025Article
- The role of SIRT1 in the development of gastrointestinal tumors.Frontiers in cell and developmental biology · 2025Review
- Therapeutic strategies for colorectal cancer: antitumor efficacy of dopamine D2 receptor antagonists.Toxicological research · 2024Review
- Novel Tetracyclic Azaphenothiazines with the Quinoline Ring as New Anticancer and Antibacterial Derivatives of Chlorpromazine.International journal of molecular sciences · 2024Article
- Propofol inhibits colon cancer cell stemness and epithelial-mesenchymal transition by regulating SIRT1, Wnt/β-catenin and PI3K/AKT/mTOR signaling pathways.Discover oncology · 2023Article
- The Role of Dopamine in Repurposing Drugs for Oncology.Biomedicines · 2023Review
- MHY2251, a New SIRT1 Inhibitor, Induces Apoptosis via JNK/p53 Pathway in HCT116 Human Colorectal Cancer Cells.Biomolecules & therapeutics · 2023Article
- Cellular and oxidative stress responses ofFrontiers in physiology · 2023Article
- Repurposed antipsychotic chlorpromazine inhibits colorectal cancer and pulmonary metastasis by inducing G2/M cell cycle arrest, apoptosis, and autophagy.Cancer chemotherapy and pharmacology · 2022Article
- Repurposing Antipsychotics for Cancer Treatment.Biomedicines · 2021Review
- Identifying FDA-approved drugs with multimodal properties against COVID-19 using a data-driven approach and a lung organoid model of SARS-CoV-2 entry.Molecular medicine (Cambridge, Mass.) · 2021Article
- Multifaceted effect of chlorpromazine in cancer: implications for cancer treatment.Oncotarget · 2021Article
- Potent efficacy of chlorpromazine in acute myeloid leukemia harboringLeukemia research reports · 2021Article
- Drug rechanneling: A novel paradigm for cancer treatment.Seminars in cancer biology · 2021Review
- Chlorpromazine eliminates acute myeloid leukemia cells by perturbing subcellular localization of FLT3-ITD and KIT-D816V.Nature communications · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Investigating existing drugs for repositioning can enable overcoming bottlenecks in the drug development process. Here, we investigated the effect and molecular mechanism of the antipsychotic drug chlorpromazine (CPZ) and identified its potential for treating colorectal cancer (CRC). Human CRC cell lines harboring different p53 statuses were used to investigate the inhibitory mechanism of CPZ. CPZ effectively inhibited tumor growth and induced apoptosis in CRC cells in a p53-dependent manner. Activation of c-jun N-terminal kinase (JNK) was crucial for CPZ-induced p53 expression and the subsequent induction of tumor apoptosis. Induction of p53 acetylation at lysine382 was involved in CPZ-mediated tumor apoptosis, and this induction was attenuated by sirtuin 1 (SIRT1), a class III histone deacetylase. By contrast, knocking down SIRT1 sensitized tumor cells to CPZ treatment. Moreover, CPZ induced the degradation of SIRT1 protein participating downstream of JNK, and JNK suppression abrogated CPZ-mediated SIRT1 downregulation. Clinical analysis revealed a significant association between high SIRT1 expression and poor outcome in CRC patients. These data suggest that SIRT1 is an attractive therapeutic target for CRC and that CPZ is a potential repositioned drug for treating CRC.
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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.