Evidence map›Paper›PMID 37572221›Full record

ArticleMolecular biotechnology2024

USP19 Negatively Regulates p53 and Promotes Cervical Cancer Progression.

Apoorvi Tyagi, Janardhan Keshav Karapurkar, Jencia Carminha Colaco, Neha Sarodaya, Ainsley Mike Antao, Kamini Kaushal, Saba Haq, Arun Pandian Chandrasekaran, Soumyadip Das, Vijai Singh and 4 more

Abstract read
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Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

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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

14 authors at 3 institutions in 2 countries.

Apoorvi TyagiGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea.
Janardhan Keshav KarapurkarGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea.
Jencia Carminha ColacoGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea.
Neha SarodayaGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea.
Ainsley Mike AntaoGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea.
Kamini KaushalGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea.
Saba HaqDepartment of Life Science, College of Natural Sciences, Hanyang University, 04763, Seoul, South Korea.
Arun Pandian ChandrasekaranGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea.
Soumyadip DasGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea.
Vijai SinghDepartment of Biosciences, School of Science, Rajpur, Indrashil University, 382715, Mehsana, Gujarat, India.
Seok-Ho HongDepartment of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea.
Bharathi SureshGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea. bharathi.suri@gmail.com.
Kye-Seong KimGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea. ks66kim@hanyang.ac.kr.
Suresh RamakrishnaGraduate School of Biomedical Science and Engineering, Hanyang University, 04763, Seoul, South Korea.ORCID http://orcid.org/0000-0002-4038-1085
Hanyang University · KRIndrashil University · INKangwon National University · KR

Funding

Korean Fund for Regenerative Medicine 22A0304L1-01Medical Research Center 2017R1A5A2015395National Research Foundation of Korea 2021M3A9H3015389National Research Foundation of Korea 2021R1I1A1A01052637
6 · The paper itself

Abstract

p53 is a tumor suppressor gene activated in response to cellular stressors that inhibits cell cycle progression and induces pro-apoptotic signaling. The protein level of p53 is well balanced by the action of several E3 ligases and deubiquitinating enzymes (DUBs). Several DUBs have been reported to negatively regulate and promote p53 degradation in tumors. In this study, we identified USP19 as a negative regulator of p53 protein level. We demonstrate a direct interaction between USP19 and p53 by pull down assay. The overexpression of USP19 promoted ubiquitination of p53 and reduced its protein half-life. We also demonstrate that CRISPR/Cas9-mediated knockout of USP19 in cervical cancer cells elevates p53 protein levels, resulting in reduced colony formation, cell migration, and cell invasion. Overall, our results indicate that USP19 negatively regulates p53 protein levels in cervical cancer progression.

Indexed as

Cell MovementDisease ProgressionTumor Suppressor Protein p53UbiquitinationUterine Cervical NeoplasmsCell Line, TumorCell ProliferationCRISPR-Cas SystemsEndopeptidasesFemaleGene Expression Regulation, NeoplasticHeLa CellsHumansEndopeptidasesTP53 protein, humanTumor Suppressor Protein p53USP19 protein, humanApoptosisDeubiquitinaseKnockoutOncogenic transformationProteolysisUbiquitination

Identifiers

PMID37572221
OpenAlexW4385780849

What Socratic 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 Socratic graph.