Evidence map›Paper›PMID 27542230›Full record

ArticleOncotarget2016

PDCD4 is a CSL associated protein with a transcription repressive function in cancer associated fibroblast activation.

Seung-Hee Jo, Dong Eun Kim, Andrea Clocchiatti, G Paolo Dotto

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Metastasis and cancer associated fibroblasts: taking it up a NOTCH.Frontiers in cell and developmental biology · 2023
    Review
  4. Article
  5. Review
  6. Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions.International journal of molecular sciences · 2019
    Review
  7. Article
  8. Article
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

4 authors at 3 institutions in 2 countries.

Seung-Hee JoCutaneous Biology Research Center, Massachusetts General Hospital, Charlestown, MA, USA.
Dong Eun KimDepartment of Biochemistry, University of Lausanne, Epalinges, CH, Switzerland.
Andrea ClocchiattiCutaneous Biology Research Center, Massachusetts General Hospital, Charlestown, MA, USA.
G Paolo DottoCutaneous Biology Research Center, Massachusetts General Hospital, Charlestown, MA, USA.
University of Lausanne · CHHarvard University · USMassachusetts General Hospital · US

Funding

GROWTH DIFFERENTIATION CONTROL IN PRIMARY KERATINOCYTES.R01AR039190 · NIAMS · YALE UNIVERSITY · PI DOTTO, GIAN-PAOLO · 1988 to 2021
$9.5M
Dermal fibroblast/ATF3 control of skin homeostasisR01AR064786 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DOTTO, GIAN-PAOLO · 2014 to 2018
$1.9M
NIAMS NIH HHS R01 AR039190NIAMS NIH HHS R01 AR064786
6 · The paper itself

Abstract

The Notch/CSL pathway plays an important role in skin homeostasis and carcinogenesis. CSL, the key effector of canonical Notch signaling endowed with an intrinsic transcription repressive function, suppresses stromal fibroblast senescence and Cancer Associated Fibroblast (CAF) activation through direct down-modulation of key effector genes. Interacting proteins that participate with CSL in this context are as yet to be identified. We report here that Programmed Cell Death 4 (PDCD4), a nuclear/cytoplasmic shuttling protein with multiple functions, associates with CSL and plays a similar role in suppressing dermal fibroblast senescence and CAF activation. Like CSL, PDCD4 is down-regulated in stromal fibroblasts of premalignant skin actinic keratosis (AKs) lesions and squamous cell carcinoma (SCC). While devoid of intrinsic DNA binding capability, PDCD4 is present at CSL binding sites of CAF marker genes as well as canonical Notch/CSL targets and suppresses expression of these genes in a fibroblast-specific manner. Thus, we propose that PDCD4 is part of the CSL repressive complex involved in negative control of stromal fibroblasts conversion into CAFs.

Indexed as

AnimalsApoptosis Regulatory ProteinsCancer-Associated FibroblastsCarcinoma, Squamous CellCell Line, TumorCellular SenescenceDown-RegulationHEK293 CellsHeLa CellsHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinKeratosis, ActinicMiceMice, SCIDProtein BindingRNA-Binding ProteinsApoptosis Regulatory ProteinsImmunoglobulin J Recombination Signal Sequence-Binding ProteinPDCD4 protein, humanRBPJ protein, humanRNA-Binding ProteinsRNA, Small InterferingCAFsNotch/CSL signalingPDCD4squamous cancertranscription repression

Identifiers

PMID27542230
PMCPMC5312270
OpenAlexW2509012192

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.