Evidence map›Paper›PMID 31474570›Full record

ReviewCancer cell2019

The Dual Roles of the Atypical Protein Kinase Cs in Cancer.

Miguel Reina-Campos, Maria T Diaz-Meco, Jorge Moscat

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. High Expression ofCancer genomics & proteomics · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. PKCActa pharmaceutica Sinica. B · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

3 authors at 2 institutions in 1 country.

Miguel Reina-CamposCancer 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.
Jorge MoscatCancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address: jmoscat@sbpdiscovery.org.
Sanford Burnham Prebys Medical Discovery Institute · USDiscovery Institute · 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

Atypical protein kinase C (aPKC) isozymes, PKCλ/ι and PKCζ, are now considered fundamental regulators of tumorigenesis. However, the specific separation of functions that determine their different roles in cancer is still being unraveled. Both aPKCs have pleiotropic context-dependent functions that can translate into tumor-promoter or -suppressive functions. Here, we review early and more recent literature to discuss how the different tumor types, and their microenvironments, might account for the selective signaling of each aPKC isotype. This is of clinical relevance because a better understanding of the roles of these kinases is essential for the design of new anti-cancer treatments.

Indexed as

AnimalsAntineoplastic AgentsCell PolarityCell Transformation, NeoplasticDisease Models, AnimalEpithelial CellsGene Expression Regulation, NeoplasticHumansIsoenzymesMice, TransgenicMutationNeoplasmsProtein Kinase CProtein Kinase C-lambdaProtein Kinase C zetaProtein Kinase InhibitorsAntineoplastic AgentsIsoenzymesProtein Kinase CProtein Kinase C-lambdaProtein Kinase C zetaProtein Kinase InhibitorsTumor Suppressor Proteinsatypical PKCsbasal cell carcinomacancercolorectal cancerECT2Hedgehogimmunotherapykinase inhibitorsleukemialung cancermetabolismp62PD-L1PHGDHPKCζPKCλ/ιpolarityprostate cancerSOX2stromatumor promotertumor suppressor

Identifiers

PMID31474570
PMCPMC6751000
OpenAlexW2970127552

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.