Evidence map›Paper›PMID 34519942›Full record

ReviewMolecular biology reports2021

Crosslink between p53 and metastasis: focus on epithelial-mesenchymal transition, cancer stem cell, angiogenesis, autophagy, and anoikis.

Ghader Babaei, Azadeh Aliarab, Mehdi Asghari Vostakolaei, Masumeh Hotelchi, Roghaiyeh Neisari, Shiva Gholizadeh-Ghaleh Aziz, Masumeh Rajabi Bazl

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  18. The senescence-associated secretory phenotype in ovarian cancer dissemination.American journal of physiology. Cell physiology · 2022
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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

7 authors at 3 institutions in 1 country.

Ghader BabaeiDepartment of Biochemistry, Faculty of Medicine, Urmia Medical Sciences University (UMSU), Urmia, Iran.ORCID http://orcid.org/0000-0003-0060-2784
Azadeh AliarabDepartment of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences(SBUMS), Tehran, Iran.ORCID http://orcid.org/0000-0003-0453-3958
Mehdi Asghari VostakolaeiDigestive Diseases Research Center, Ardabil University of Medical Sciences, Ardabil, Iran.ORCID http://orcid.org/0000-0002-4732-8105
Masumeh HotelchiDepartment of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences(SBUMS), Tehran, Iran.ORCID http://orcid.org/0000-0002-4356-5410
Roghaiyeh NeisariShahid Motahhari Hospital, Urmia University of Medical Science, Urmia, Iran.ORCID http://orcid.org/0000-0002-2735-8497
Shiva Gholizadeh-Ghaleh AzizDepartment of Biochemistry, Faculty of Medicine, Urmia Medical Sciences University (UMSU), Urmia, Iran. gholizadeh.sh@umsu.ac.ir.ORCID http://orcid.org/0000-0003-1949-4381
Masumeh Rajabi BazlDepartment of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences(SBUMS), Tehran, Iran. rajabi_m@sbmu.ac.ir.ORCID http://orcid.org/0000-0002-9720-5904
Shahid Beheshti University of Medical Sciences · IRUrmia University · IRArdabil University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionP53, as a tumor suppressor gene, is believed to be one of the most mutated genes in cancer cells. The mutant forms of this protein often play a tumorigenic role in cancer cells. Recent evidence shows that p53 plays a critical role in the migration, metastasis, and invasion of cancer cells. The present article aims to investigate the molecular mechanism that induces metastasis in cancer cells generated by the mutant P53, and to highlight the compounds targeting mutant-p53 together with their clinical applications.

methodsA detailed literature search was conducted to find information about the role of the mutant-p53 in the processes involved in metastasis in various databases.

resultsA growing body of evidence suggests that Mutant-p53 enhances tumor metastasis affecting the Epithelial-mesenchymal transition (EMT) process, cancer stem cells, angiogenesis, autophagy, anoikis, and any other mechanisms regarding metastasis.

conclusionsTaken together, targeting mutant-p53 by altering the processes involved in metastasis could be a potential therapeutic strategy in the treatment of metastatic cancer.

Indexed as

AnoikisAutophagyEpithelial-Mesenchymal TransitionHumansNeoplasm MetastasisNeoplasmsNeoplastic Stem CellsNeovascularization, PathologicTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53AngiogenesisAnoikisAutophagyCancer stem cellsEMTMetastasisMutant p53

Identifiers

PMID34519942
OpenAlexW3200489044

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.