ArticleJournal of experimental & clinical cancer research : CR2021
Targeting INMT and interrupting its methylation pathway for the treatment of castration resistant prostate cancer.
Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- High-Dose Voclosporin Protects Against Acute Kidney Injury via Regnase-2-Mediated NGAL MRNA Decay.International journal of molecular sciences · 2026Article
- Cross-cohort multi-omics analysis identifies novel clusters driven by epithelial-mesenchymal transition signatures in gastric cancer.Cancer cell international · 2026Article
- Epigenetic regulation of TIPE3 in nasopharyngeal carcinoma and its impact on the hedgehog signaling pathway.Cellular and molecular life sciences : CMLS · 2025Article
- Voclosporin Overdose-Induced Peroxisomal Structural Changes and AKI Are Prevented by Renal Indole Detoxifier, INMT.Journal of the American Society of Nephrology : JASN · 2025Article
- Metabolic heterogeneity and survival outcomes in papillary renal cell carcinoma: insights from multi-datasets and machine learning analyses.Hereditas · 2025Article
- Implications of Indolethylamine N-Methyltransferase (INMT) in Health and Disease: Biological Functions, Disease Associations, Inhibitors, and Analytical Approaches.Brain sciences · 2025Review
- Bolstering CD8Biology · 2025Review
- Article
- Cellular Signaling of Amino Acid Metabolism in Prostate Cancer.International journal of molecular sciences · 2025Review
- GD-Net: An Integrated Multimodal Information Model Based on Deep Learning for Cancer Outcome Prediction and Informative Feature Selection.Journal of cellular and molecular medicine · 2024Article
- β-hydroxybutyrate inhibits malignant phenotypes of prostate cancer cells through β-hydroxybutyrylation of indoleacetamide-N-methyltransferase.Cancer cell international · 2024Article
- Molecular landscape for risk prediction and personalized therapeutics of castration-resistant prostate cancer: at a glance.Frontiers in endocrinology · 2024Review
- Discovery of a small-molecule NDR1 agonist for prostate cancer therapy.Frontiers in pharmacology · 2024Article
- Development and validation of a selenium metabolism regulators associated prognostic model for hepatocellular carcinoma.BMC cancer · 2023Article
- Choosing Kinase Inhibitors for Androgen Deprivation Therapy-Resistant Prostate Cancer.Pharmaceutics · 2022Review
- Low expression of INMT is associated with poor prognosis but favorable immunotherapy response in lung adenocarcinoma.Frontiers in genetics · 2022Article
- Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance.Journal of clinical medicine · 2021Review
- Cancer Chemoprevention: A Strategic Approach Using Phytochemicals.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCastration-resistant prostate cancer (CRPC) is associated with a very poor prognosis, and the treatment of which remains a serious clinical challenge.
methodsRNA-seq, qPCR, western blot and immunohistochemistry were employed to identify and confirm the high expression of indolethylamine N-methyltransferase (INMT) in CRPC and the clinical relevance. Chip assay was used to identify Histone-Lysine N-Methyltransferase (SMYD3) as a major epigenetic regulator of INMT. LC-MS/MS were used to identify new substrates of INMT methylation in CRPC tissues. Gene knockdown/overexpression, MTT and mouse cancer models were used to examine the role of INMT as well as the anticancer efficacy of INMT inhibitor N,N-dimethyltryptamine (DMT), the SMYD3 inhibitor BCl-12, the selenium compounds methaneseleninic acid (MSA) and Se-(Methyl)selenocysteine hydrochloride (MSC), and the newly identified endogenous INMT substrate Bis(7)-tacrine.
resultsWe found that the expression of INMT was highly increased in CRPC and was correlated with poor prognosis of clinical prostate cancer (PCa). INMT promoted PCa castration resistance via detoxification of anticancer metabolites. Knockdown of INMT or treatment with INMT inhibitor N,N-dimethyltryptamine (DMT) significantly suppressed CRPC development. Histone-Lysine N-Methyltransferase SMYD3 was a major epigenetic regulator of INMT expression, treatment with SMYD3 inhibitor BCl-121 suppressed INMT expression and inhibits CRPC development. Importantly, INMT knockdown significantly increased the anticancer effect of the exogenous selenium compounds methaneseleninic acid (MSA) and Se-(Methyl)selenocysteine hydrochloride (MSC) as well as the endogenous metabolite Bis(7)-tacrine.
conclusionsOur study suggests that INMT drives PCa castration resistance through detoxification of anticancer metabolites, targeting INMT or its regulator SMYD3 or/and its methylation metabolites represents an effective therapeutic avenue for CRPC treatment.
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