ArticleACS central science2023
New Pathway for Cisplatin Prodrug to Utilize Metabolic Substrate Preference to Overcome Cancer Intrinsic Resistance.
Article in ACS central science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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
14 citing papers in PubMed, 24 citations in OpenAlex.
- SPINK5 promotes sensitivity to cisplatin by inducing ferroptosis in head and neck carcinoma.Cancer gene therapy · 2026Article
- Molecular Insights into the Incorporation of Platinum-Based Drugs into Lipid Aggregates.ACS omega · 2026Article
- Protective Role of Linagliptin in Cisplatin-Mediated Liver Injury: Involvement of STAT3 and AMPK/SIRT1/PGC-1alpha Mitochondrial Energy Sensing Networks.Advances in pharmacological and pharmaceutical sciences · 2026Article
- Emerging roles for fatty acid oxidation in cancer.Genes & diseases · 2025Review
- Identification and validation of platinum resistance signature in gastric cancer.Cancer cell international · 2025Article
- PEGylation Effects on Amphiphilic Platinum(IV) Complexes: Influence on Uptake, Activation, and Cytotoxicity.Pharmaceutics · 2025Article
- Article
- A Dual Action Platinum(IV) Complex with Self-assembly Property Inhibits Prostate Cancer through Mitochondrial Stress Pathway.ChemMedChem · 2024Article
- Lipid Metabolism Modulatory Cisplatin Prodrug Sensitizes Resistant Prostate Cancer toward Androgen Deprivation Therapy.ACS pharmacology & translational science · 2024Article
- Simultaneous targeting of peripheral and brain tumors with a therapeutic nanoparticle to disrupt metabolic adaptability at both sites.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Nanocarrier-mediated cancer therapy with cisplatin:Heliyon · 2024Article
- Platin-L improves cisplatin resistance.Nature reviews. Urology · 2023Article
- Repurposing Platinum(IV) Prodrugs to Modulate Mitochondrial Metabolism.ACS central science · 2023Article
- Unlocking the role of non-coding RNAs in prostate cancer progression: exploring the interplay with the Wnt signaling pathway.Frontiers in pharmacology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Tumor cells adapt to diverse survival strategies defying our pursuit of multimodal cancer therapy. Prostate cancer (PCa) is an example that is resistant to one of the most potent chemotherapeutics, cisplatin. PCa cells survive and proliferate using fatty acid oxidation (FAO), and the dependence on fat utilization increases as the disease progresses toward a resistant form. Using a pool of patient biopsies, we validated the expression of a key enzyme carnitine palmitoyltransferase 1 A (CPT1A) needed for fat metabolism. We then discovered that a cisplatin prodrug, Platin-L, can inhibit the FAO of PCa cells by interacting with CPT1A. Synthesizing additional cisplatin-based prodrugs, we documented that the presence of an available carboxylic acid group near the long chain fatty acid linker on the Pt(IV) center is crucial for CPT1A binding. As a result of fat metabolism disruption by Platin-L, PCa cells transition to an adaptive glucose-dependent chemosensitive state. Potential clinical translation of Platin-L will require a delivery vehicle to direct it to the prostate tumor microenvironment. Thus, we incorporated Platin-L in a biodegradable prostate tumor-targeted orally administrable nanoformulation and demonstrated its safety and efficacy. The distinctive FAO inhibitory property of Platin-L can be of potential clinical relevance as it offers the use of cisplatin for otherwise resistant cancer.
Identifiers
What Socratic 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 Socratic graph.