Evidence map›Paper›PMID 37877353›Full record

ArticleClinical and translational medicine2023

Parkin regulates IGF2BP3 through ubiquitination in the tumourigenesis of cervical cancer.

Xin Sun, Guiqin Ye, Jiuzhou Li, Huafeng Shou, Gongxun Bai, Jianbin Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 17 citations in OpenAlex.

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  18. Epitranscriptomics and cervical cancer: the emerging role of mExpert reviews in molecular medicine · 2024
    Review
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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

6 authors at 4 institutions in 1 country.

Xin SunDepartment of Medical Oncology, Cancer Center, Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, China.
Guiqin YeBasic Medical Sciences, Hangzhou Medical College, Hangzhou, China.
Jiuzhou LiDepartment of Neurosurgery, Binzhou People's Hospital, Binzhou, China.
Huafeng ShouDepartment of Gynecology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Binzhou, China.
Gongxun BaiKey Laboratory of Rare Earth Optoelectronic Materials and Devices of Zhejiang Province, College of Optical and Electronic Technology, China Jiliang University, Hangzhou, China.
Jianbin ZhangDepartment of Medical Oncology, Cancer Center, Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, China.ORCID 0000-0001-6256-2293
Zhejiang Provincial People's Hospital · CNBinzhou People's Hospital · CNChina Jiliang University · CNHangzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin-like growth Factor 2 mRNA-binding protein 3 (IGF2BP3) is a highly conserved RNA-binding protein and plays a critical role in regulating posttranscriptional modifications.

methodsImmunoprecipitation was used to examine the interaction of Parkin and IGF2BP3. Mass spectrometry was performed to identify the ubiquitination sites of IGF2BP3. RNA-immunoprecipitation was conducted to examine the target genes of IGF2BP3. Xenograft mouse model was constructed to determine the tumorigenesis of IGF2BP3.

resultsIGF2BP3 expression is negatively correlated with Parkin expression in human cervical cancer cells and tissues. Parkin directly interacts with IGF2BP3, and overexpression of Parkin causes the proteasomal degradation of IGF2BP3, while knockdown of PARK2 increases the protein levels of IGF2BP3. Mechanistically, in vivo and in vitro ubiquitination assays demonstrated that Parkin is able to ubiquitinate IGF2BP3. Moreover, the ubiquitination site of IGF2BP3 was identified at K213 in the first KH domain of IGF2BP3. IGF2BP3 mutation results in the loss of its oncogenic function as an m6A reader, resulting in the inactivation of the phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signalling pathways. In addition, IGF2BP3 mutation results in the attenuation of Parkin-mediated mitophagy, indicating its inverse role in regulating Parkin. Consequently, the tumourigenesis of cervical cancer is also inhibited by IGF2BP3 mutation.

conclusionIGF2BP3 is ubiquitinated and regulated by the E3 ubiquitin ligase Parkin in human cervical cancer and ubiquitination modification plays an important role in modulating IGF2BP3 function. Thus, understanding the role of IGF2BP3 in tumourigenesis could provide new insights into cervical cancer therapy.

Indexed as

Phosphatidylinositol 3-KinasesRNA-Binding ProteinsUbiquitin-Protein LigasesUterine Cervical NeoplasmsAnimalsCarcinogenesisFemaleHumansMiceUbiquitinationIGF2BP3 protein, humanparkin proteinPhosphatidylinositol 3-KinasesRNA-Binding ProteinsUbiquitin-Protein Ligasescervical cancerIGF2BP3mitophagyparkinubiquitination

Identifiers

PMID37877353
PMCPMC10599278
OpenAlexW4387931397

What OpenQuestion holds

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Registered trials

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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.