Evidence map›Paper›PMID 32920697›Full record

ReviewCellular and molecular life sciences : CMLS2021

Interplay between HMGA and TP53 in cell cycle control along tumor progression.

Nathalia Meireles Da Costa, Antonio Palumbo, Marco De Martino, Alfredo Fusco, Luis Felipe Ribeiro Pinto, Luiz Eurico Nasciutti

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. NAT10 Promotes Prostate Cancer Growth and Metastasis by Acetylating mRNAs of HMGA1 and KRT8.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Network Pharmacology-Based Study on the Mechanism of Aloe Vera for Treating Cancer.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  13. 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

6 authors at 3 institutions in 2 countries.

Nathalia Meireles Da CostaPrograma de Carcinogênese Molecular, Instituto Nacional de Câncer-INCA, Rua André Cavalcanti, 37-6th floor-Centro, 20231-050, Rio de Janeiro, RJ, Brazil. nathalia.meireles@inca.gov.br.ORCID http://orcid.org/0000-0002-7528-519X
Antonio PalumboLaboratório de Interações Celulares, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro Prédio de Ciências da Saúde-Cidade Universitária, Ilha do Fundão, A. Carlos Chagas, 373-Bloco F, Sala 26, 21941-902, Rio de Janeiro, RJ, Brazil.ORCID http://orcid.org/0000-0002-7977-8522
Marco De MartinoIstituto di Endocrinologia e Oncologia Sperimentale-CNR c/o Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli "Federico II", Naples, Italy.
Alfredo FuscoIstituto di Endocrinologia e Oncologia Sperimentale-CNR c/o Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli "Federico II", Naples, Italy.
Luis Felipe Ribeiro PintoPrograma de Carcinogênese Molecular, Instituto Nacional de Câncer-INCA, Rua André Cavalcanti, 37-6th floor-Centro, 20231-050, Rio de Janeiro, RJ, Brazil.ORCID http://orcid.org/0000-0001-5509-1008
Luiz Eurico NasciuttiLaboratório de Interações Celulares, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro Prédio de Ciências da Saúde-Cidade Universitária, Ilha do Fundão, A. Carlos Chagas, 373-Bloco F, Sala 26, 21941-902, Rio de Janeiro, RJ, Brazil. luiz.nasciutti@histo.ufrj.br.
Institute for Experimental Endocrinology and Oncology · ITInstituto Nacional de Câncer - INCA · BRUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The high mobility group A (HMGA) proteins are found to be aberrantly expressed in several tumors. Studies (in vitro and in vivo) have shown that HMGA protein overexpression has a causative role in carcinogenesis process. HMGA proteins regulate cell cycle progression through distinct mechanisms which strongly influence its normal dynamics along malignant transformation. Tumor protein p53 (TP53) is the most frequently altered gene in cancer. The loss of its activity is recognized as the fall of a barrier that enables neoplastic transformation. Among the different functions, TP53 signaling pathway is tightly involved in control of cell cycle, with cell cycle arrest being the main biological outcome observed upon p53 activation, which prevents accumulation of damaged DNA, as well as genomic instability. Therefore, the interaction and opposing effects of HMGA and p53 proteins on regulation of cell cycle in normal and tumor cells are discussed in this review. HMGA proteins and p53 may reciprocally regulate the expression and/or activity of each other, leading to the counteraction of their regulation mechanisms at different stages of the cell cycle. The existence of a functional crosstalk between these proteins in the control of cell cycle could open the possibility of targeting HMGA and p53 in combination with other therapeutic strategies, particularly those that target cell cycle regulation, to improve the management and prognosis of cancer patients.

Indexed as

Cell Cycle CheckpointsDisease ProgressionDNA DamageGene Expression Regulation, NeoplasticGenomic InstabilityHMGA ProteinsHumansNeoplasmsSignal TransductionTumor Suppressor Protein p53HMGA ProteinsTumor Suppressor Protein p53CancerCell cycleCell cycle-directed anti-cancer therapiesHMGATP53

Identifiers

PMID32920697
PMCPMC11071717
OpenAlexW3086905834

What OpenQuestion holds

Textmetadata
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.