Evidence map›Paper›PMID 30827887›Full record

ArticleCancer cell2019

Increased Serine and One-Carbon Pathway Metabolism by PKCλ/ι Deficiency Promotes Neuroendocrine Prostate Cancer.

Miguel Reina-Campos, Juan F Linares, Angeles Duran, Thekla Cordes, Antoine L'Hermitte, Mehmet G Badur, Munveer S Bhangoo, Phataraporn K Thorson, Alicia Richards, Tarmo Rooslid and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed
17.4field-weighted citation impact, top 1% of its field
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

131 citing papers in PubMed, 179 citations in OpenAlex.

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  16. PMA exerts anti-leukemia effect in PhCancer cell international · 2025
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71 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 10 institutions in 2 countries.

Miguel Reina-CamposCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA; Sanford Burnham Prebys Graduate School of Biomedical Sciences, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Juan F LinaresCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Angeles DuranCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Thekla CordesDepartment of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA.
Antoine L'HermitteCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Mehmet G BadurDepartment of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA.
Munveer S BhangooDivision of Hematology-Oncology Scripps Clinic, 10666 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Phataraporn K ThorsonDepatment of Pathology, Scripps Clinic Medical Group, 10666 Torrey Pines Road, La Jolla, CA 92037, USA.
Alicia RichardsProteomics Facility, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Tarmo RooslidConrad Prebys Center for Drug Discovery, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Dolores C Garcia-OlmoCentre de Recerca Experimental Biomèdica Aplicada (CREBA), IRBLLEIDA, 25138 Lleida, Spain.
Syongh Y Nam-ChaPathology Department, Director of the Research Unit Biobank, University of Castilla-La Mancha, School of Medicine, 02006 Albacete, Spain.
Antonio S Salinas-SanchezUrology Department, Research Unit, University Hospital Complex of Albacete, School of Medicine, 02006 Albacete, Spain.
Ken EngDepartment of Computational Biomedicine, Weill Cornell Medicine, New York, NY 10065, USA.
Himisha BeltranDepartment of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
David A ScottCancer Metabolism Core, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Christian M MetalloDepartment of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA.
Jorge MoscatCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Maria T Diaz-MecoCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address: mdmeco@sbpdiscovery.org.
Discovery Institute · USUniversity of California, San Diego · USSanford Burnham Prebys Medical Discovery Institute · USBiomedical Research Institute of Lleida · ESHarvard University · USHospital General Universitario de Albacete · ESScripps Clinic · USScripps Clinic Medical Group · USUniversity of Castilla-La Mancha · ESWeill Cornell Medicine · US

Funding

Role of p62/SQSTM1 in obesity-induced liver cancerR01CA211794 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KARIN, MICHAEL, MOSCAT, JORGE · 2017 to 2021
$3.6M
Role of p62 in metabolic reprograming of the tumor stroma in prostate cancerR01CA218254 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DIAZ MECO CONDE, MARIA TERESA, METALLO, CHRISTIAN MICHAEL · 2017 to 2021
$2.6M
The p62/MEKK3 complex in mTORC1 activationR01CA192642 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI DIAZ MECO CONDE, MARIA TERESA · 2015 to 2019
$2.2M
Control of stellate cells-driven liver cancer by the p62/NBR1 adaptersR01DK108743 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI MOSCAT, JORGE · 2016 to 2020
$2.2M
Mechanisms of cell death and autophagy in intestinal epithelial cells in inflammation and cancerR01CA207177 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MOSCAT, JORGE · 2017 to 2021
$2.1M
NCI NIH HHS R01 CA192642NCI NIH HHS R01 CA207177NCI NIH HHS R01 CA211794NCI NIH HHS R01 CA218254NIDDK NIH HHS R01 DK108743
6 · The paper itself

Abstract

Increasingly effective therapies targeting the androgen receptor have paradoxically promoted the incidence of neuroendocrine prostate cancer (NEPC), the most lethal subtype of castration-resistant prostate cancer (PCa), for which there is no effective therapy. Here we report that protein kinase C (PKC)λ/ι is downregulated in de novo and during therapy-induced NEPC, which results in the upregulation of serine biosynthesis through an mTORC1/ATF4-driven pathway. This metabolic reprogramming supports cell proliferation and increases intracellular S-adenosyl methionine (SAM) levels to feed epigenetic changes that favor the development of NEPC characteristics. Altogether, we have uncovered a metabolic vulnerability triggered by PKCλ/ι deficiency in NEPC, which offers potentially actionable targets to prevent therapy resistance in PCa.

Indexed as

Down-RegulationActivating Transcription Factor 4Biosynthetic PathwaysCarcinoma, NeuroendocrineCell Line, TumorDNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansIsoenzymesMaleMechanistic Target of Rapamycin Complex 1Prostatic NeoplasmsProtein Kinase CProtein Kinase C-lambdaS-AdenosylmethionineActivating Transcription Factor 4ATF4 protein, humanIsoenzymesMechanistic Target of Rapamycin Complex 1Protein Kinase CProtein Kinase C-lambdaS-AdenosylmethionineSerineaPKCATF4cancer metabolismepigeneticslineage plasticitymTORneuroendocrinePKClambdaprostate cancerserine metabolism

Identifiers

PMID30827887
PMCPMC6424636
OpenAlexW2918028648

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.