ArticleBritish journal of cancer2026
Adipose triglyceride lipase driven lipolysis as a targetable metabolic vulnerability in prostate cancer with intrinsic metabolic inflexibility.
Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Vitronectin Enrichment in Prostate Cancer Liver Metastases Promotes Adhesion and Survival.Cancer research communications · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite the widespread clinical use of prostate-specific membrane antigen (PSMA)-targeted imaging and therapy in prostate cancer, the biological functions underlying PSMA-associated tumour aggressiveness remain incompletely understood.
methodsPSMA-PET-guided sampling of paired PSMA-high and PSMA-low tumour regions was used for integrated proteomic and epigenomic analyses. PSMA-ATGL correlation was validated by immunohistochemistry in 90 treatment-naïve patients. Metabolic profiling was performed using Seahorse Mito Fuel Flex Test assays under unperturbed conditions and pharmacological or genetic perturbation of ATGL and PSMA. Therapeutic vulnerability was assessed using NG-497 and siRNA-mediated knockdown.
resultsPSMA-high tumours exhibited lipolytic reprogramming characterised by ATGL upregulation, confirmed by a robust PSMA-ATGL correlation in the validation cohort (P < 0.0001). Despite shared fatty acid dependency, LNCaP cells exhibited intrinsic metabolic inflexibility while 22RV1 cells displayed high adaptability. Both pharmacological and genetic ATGL inhibition most potently impaired LNCaP proliferation. Enzalutamide upregulated ATGL in both cell lines, revealing reciprocal regulation between AR signaling and the PSMA/ATGL axis.
conclusionsATGL-mediated lipolysis represents a promising therapeutic target in prostate cancer, with heightened sensitivity in tumours lacking metabolic flexibility to utilize alternative pathways.
Identifiers
42493599What 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.