Evidence map›Paper›PMID 33253914›Full record

ReviewCellular signalling2021

Dysregulation of lysophospholipid signaling by p53 in malignant cells and the tumor microenvironment.

Sue Chin Lee, Kuan-Hung Lin, Andrea Balogh, Derek D Norman, Mitul Bavaria, Bryan Kuo, Junming Yue, Louisa Balázs, Zoltán Benyó, Gábor Tigyi

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. E2F7 drives autotaxin/Enpp2 transcription via chromosome looping: Repression by p53 in murine but not in human carcinomas.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  5. Generation and multiomic profiling of aScience translational medicine · 2022
    Article
  6. 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

10 authors at 2 institutions in 2 countries.

Sue Chin LeeDepartment of Physiology, University of Tennessee Health Science Center Memphis, Van Vleet Cancer Research Building, 3 N. Dunlap Street, Memphis, TN 38163, USA.
Kuan-Hung LinDepartment of Physiology, University of Tennessee Health Science Center Memphis, Van Vleet Cancer Research Building, 3 N. Dunlap Street, Memphis, TN 38163, USA.
Andrea BaloghDepartment of Physiology, University of Tennessee Health Science Center Memphis, Van Vleet Cancer Research Building, 3 N. Dunlap Street, Memphis, TN 38163, USA; Institute of Translational Medicine, Semmelweis University, POB 2, H-1428 Budapest, Hungary.
Derek D NormanDepartment of Physiology, University of Tennessee Health Science Center Memphis, Van Vleet Cancer Research Building, 3 N. Dunlap Street, Memphis, TN 38163, USA.
Mitul BavariaDepartment of Physiology, University of Tennessee Health Science Center Memphis, Van Vleet Cancer Research Building, 3 N. Dunlap Street, Memphis, TN 38163, USA.
Bryan KuoDepartment of Physiology, University of Tennessee Health Science Center Memphis, Van Vleet Cancer Research Building, 3 N. Dunlap Street, Memphis, TN 38163, USA.
Junming YueDepartment of Pathology, University of Tennessee Health Science Center Memphis, USA.
Louisa BalázsDepartment of Pathology, University of Tennessee Health Science Center Memphis, USA.
Zoltán BenyóInstitute of Translational Medicine, Semmelweis University, POB 2, H-1428 Budapest, Hungary.
Gábor TigyiDepartment of Physiology, University of Tennessee Health Science Center Memphis, Van Vleet Cancer Research Building, 3 N. Dunlap Street, Memphis, TN 38163, USA; Institute of Translational Medicine, Semmelweis University, POB 2, H-1428 Budapest, Hungary. Electronic address: gtigyi@uthsc.edu.
University of Tennessee Health Science Center · USSemmelweis University · HU

Funding

Preclinical Evaluation of Radioprotectin-1 for Mitigation of GI-ARSU19AI150574 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI TERRIN, MICHAEL L · 2020 to 2024
$13.0M
Ligand Recognition by Phospholipid Growth Factor ReceptorsR01CA092160 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI TIGYI, GABOR J · 2001 to 2022
$5.9M
IND-Enabling Preclinical Development of a New RadiomitigatorU01AI107331 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI TIGYI, GABOR J · 2013 to 2018
$2.9M
NCI NIH HHS R01 CA092160NIAID NIH HHS U01 AI107331NIAID NIH HHS U19 AI150574
6 · The paper itself

Abstract

The TP53 gene has been widely studied for its roles in cell cycle control, maintaining genome stability, activating repair mechanisms upon DNA damage, and initiating apoptosis should repair mechanisms fail. Thus, it is not surprising that mutations of p53 are the most common genetic alterations found in human cancer. Emerging evidence indicates that dysregulation of lipid metabolism by p53 can have a profound impact not only on cancer cells but also cells of the tumor microenvironment (TME). In particular, intermediates of the sphingolipid and lysophospholipid pathways regulate many cellular responses common to p53 such as cell survival, migration, DNA damage repair and apoptosis. The majority of these cellular events become dysregulated in cancer as well as cell senescence. In this review, we will provide an account on the seminal contributions of Prof. Lina Obeid, who deciphered the crosstalk between p53 and the sphingolipid pathway particularly in modulating DNA damage repair and apoptosis in non-transformed as well as transformed cells. We will also provide insights on the integrative role of p53 with the lysophosphatidic acid (LPA) signaling pathway in cancer progression and TME regulation.

Indexed as

Signal TransductionTumor MicroenvironmentHumansLysophospholipidsNeoplasmsTumor Suppressor Protein p53lysophosphatidic acidLysophospholipidsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID33253914
PMCPMC7967251
OpenAlexW3108084595

What OpenQuestion 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 OpenQuestion graph.