Evidence map›Paper›PMID 40383250›Full record

ArticleBiochimica et biophysica acta. Molecular and cell biology of lipids2025

DHA suppresses hormone-sensitive and castration-resistant prostate cancer growth by decreasing de novo lipogenesis.

G H Tamarindo, C F Ribeiro, S Rodrigues, R M Góes, M Loda

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In one paragraph

Article in Biochimica et biophysica acta. Molecular and cell biology of lipids, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

G H TamarindoInstitute of Biology, University of Campinas, Campinas, São Paulo, Brazil; Brazilian Biosciences National Laboratory, Brazilian Center for Research in Energy and Materials (CNPEM), Campinas, São Paulo, Brazil; Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, Cornell University, New York, United States of America.
C F RibeiroDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, Cornell University, New York, United States of America.
S RodriguesDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, Cornell University, New York, United States of America.
R M GóesInstitute of Biology, University of Campinas, Campinas, São Paulo, Brazil; Department of Biology, Institute of Biosciences, Humanities and Exact Sciences, São Paulo State University, São Paulo, Brazil.
M LodaDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, Cornell University, New York, United States of America; Department of Oncologic Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States of America; Nuffield Department of Surgical Sciences, Lincoln College, University of Oxford, Oxford, UK. Electronic address: mloda@med.cornell.edu.

Funding

Tumor and Circulating Markers as Links Between Obesity and Lethal Prostate CanceP50CA090381 · NCI · DANA-FARBER CANCER INSTITUTE · PI KANTOFF, PHILIP W · 2002 to 2017
$36.2M
Weill Cornell Medicine (WCM) SPORE in Prostate CancerP50CA211024 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GUDAS, LORRAINE J · 2017 to 2021
$10.9M
Molecular Link Between Metabolic Syndrome and Prostate CancerR01CA131945 · NCI · DANA-FARBER CANCER INST · PI LODA, MASSIMO · 2008 to 2018
$4.0M
NCI NIH HHS P50 CA090381NCI NIH HHS P50 CA211024NCI NIH HHS R01 CA131945
6 · The paper itself

Abstract

objectiveDe novo lipogenesis (DNL) is associated with prostate cancer (PCa) progression, while fatty acid synthase (FASN) overexpression is a hallmark of DNL. Palmitate, its main product, is a saturated fatty acid that supports PCa growth. Polyunsaturated fatty acids (PUFAs), which can be acquired from the microenvironment, undergo peroxidation more readily and affect membrane fluidity. Docosahexaenoic acid (DHA) is a prototype PUFA omega-3 produced inefficiently in human cells. Its levels are low in PCa cells compared to normal cells. We hypothesize that excess DHA may reprogram lipid metabolism and induce cell growth suppression.

methodsAndrogen-responsive LNCaP, castration-resistant cells C4-2 and 22Rv1, human PCa castration-resistant organoids, and prostate cancer xenografts were exposed to DHA.

resultsDHA accumulated into lipid droplets as triacylglycerols and cholesterol esters, led to increased phospholipid acyl chain unsaturation and altered phospholipid ratio, a known trigger of endoplasmic reticulum (ER) stress. DHA caused a decrease in sterol regulatory element-binding protein (SREBP) transcriptional program, which, in turn, led to decreased expression of FASN. The subsequent reduction in DNL caused downregulation of the androgen receptor (AR) and its splice variant AR-V7. In addition, β-oxidation was enhanced, and DHA was preferentially oxidized over palmitate. Glucose oxidation also increased in the presence of DHA. Finally, DHA led to ROS overproduction, oxidative damage, and ER stress.

conclusionsDHA reduces the growth of hormone-sensitive and castration-resistant PCa both in vitro and in vivo via deregulation of lipid metabolism.

Indexed as

Docosahexaenoic AcidsLipogenesisProstatic Neoplasms, Castration-ResistantAnimalsCell Line, TumorCell ProliferationFatty Acid Synthase, Type IHumansLipid MetabolismMaleMiceReceptors, AndrogenXenograft Model Antitumor AssaysDocosahexaenoic AcidsFASN protein, humanFatty Acid Synthase, Type IReceptors, AndrogenDHAOmega-3Prostate cancer;lipids

Identifiers

PMID40383250
PMCPMC13600599

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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.