Evidence map›Paper›PMID 34957087›Full record

ReviewFrontiers in cell and developmental biology2021

Regulation of miRNAs Expression by Mutant p53 Gain of Function in Cancer.

Tzitzijanik Madrigal, Jesús Hernández-Monge, Luis A Herrera, Claudia Haydée González-De la Rosa, Guadalupe Domínguez-Gómez, Myrna Candelaria, Fernando Luna-Maldonado, Karla G Calderón González, José Díaz-Chávez

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 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
1.1field-weighted citation impact, top 25% 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, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. How MicroRNAs Command the Battle against Cancer.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  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

9 authors at 4 institutions in 1 country.

Tzitzijanik MadrigalUnidad de Investigación Biomédica en Cáncer, Instituto de Investigaciones Biomédicas, UNAM/Instituto Nacional de Cancerología, Mexico City, Mexico.
Jesús Hernández-MongeCátedra-CONACyT Laboratorio de Biomarcadores Moleculares, Instituto de Física, UASLP, San Luis Potosí, Mexico.
Luis A HerreraUnidad de Investigación Biomédica en Cáncer, Instituto de Investigaciones Biomédicas, UNAM/Instituto Nacional de Cancerología, Mexico City, Mexico.
Claudia Haydée González-De la RosaDepartamento de Ciencias Naturales, Unidad Cuajimalpa, Universidad Autónoma Metropolitana, Mexico City, Mexico.
Guadalupe Domínguez-GómezSubdirección de Investigación Clínica, Instituto Nacional de Cancerología, Mexico City, Mexico.
Myrna CandelariaSubdirección de Investigación Clínica, Instituto Nacional de Cancerología, Mexico City, Mexico.
Fernando Luna-MaldonadoUnidad de Investigación Biomédica en Cáncer, Instituto de Investigaciones Biomédicas, UNAM/Instituto Nacional de Cancerología, Mexico City, Mexico.
Karla G Calderón GonzálezLaboratorio de Interacciones Biomoleculares y Cáncer, Instituto de Física, UASLP, San Luis Potosi, Mexico.
José Díaz-ChávezUnidad de Investigación Biomédica en Cáncer, Instituto de Investigaciones Biomédicas, UNAM/Instituto Nacional de Cancerología, Mexico City, Mexico.
Instituto Nacional de Cancerología · MXAutonomous University of San Luis Potosí · MXNational Institute of Genomic Medicine · MXUniversidad Autónoma Metropolitana · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 roles have been largely described; among them, cell proliferation and apoptosis control are some of the best studied and understood. Interestingly, the mutations on the six hotspot sites within the region that encodes the DNA-binding domain of p53 give rise to other very different variants. The particular behavior of these variants led to consider p53 mutants as separate oncogene entities; that is, they do not retain wild type functions but acquire new ones, namely Gain-of-function p53 mutants. Furthermore, recent studies have revealed how p53 mutants regulate gene expression and exert oncogenic effects by unbalancing specific microRNAs (miRNAs) levels that provoke epithelial-mesenchymal transition, chemoresistance, and cell survival, among others. In this review, we discuss recent evidence of the crosstalk between miRNAs and mutants of p53, as well as the consequent cellular processes dysregulated.

Indexed as

cancergain of functionmiRNA biogenesismiRNAsmutant p53

Identifiers

PMID34957087
PMCPMC8697023
OpenAlexW4226250332

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.