Evidence map›Paper›PMID 35064108›Full record

ArticleCell death & disease2022

HERC3 regulates epithelial-mesenchymal transition by directly ubiquitination degradation EIF5A2 and inhibits metastasis of colorectal cancer.

Zhiyuan Zhang, Guodong He, Yang Lv, Yu Liu, Zhengchuan Niu, Qingyang Feng, Ronggui Hu, Jianmin Xu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. 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
2.7field-weighted citation impact, top 9% 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, 33 citations in OpenAlex.

  1. Article
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  5. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025
    Review
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  12. The cross talk of ubiquitination and chemotherapy tolerance in colorectal cancer.Journal of cancer research and clinical oncology · 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

8 authors at 2 institutions in 1 country.

Zhiyuan Zhang *Department of General Surgery, Zhongshan Hospital, Fudan University, 200030, Shanghai, China.ORCID 0000-0003-0336-7783
Guodong He *Department of General Surgery, Zhongshan Hospital, Fudan University, 200030, Shanghai, China.
Yang Lv *Department of General Surgery, Zhongshan Hospital, Fudan University, 200030, Shanghai, China.
Yu Liu *Department of General Surgery, Zhongshan Hospital, Fudan University, 200030, Shanghai, China.
Zhengchuan Niu *Department of General Surgery, Zhongshan Hospital, Fudan University, 200030, Shanghai, China.
Qingyang FengDepartment of General Surgery, Zhongshan Hospital, Fudan University, 200030, Shanghai, China.
Ronggui HuState Key Laboratory of Molecular Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, 200030, Shanghai, China. coryhu00@gmail.com.ORCID 0000-0002-3939-6087
Jianmin XuDepartment of General Surgery, Zhongshan Hospital, Fudan University, 200030, Shanghai, China. xujmin@aliyun.com.ORCID 0000-0002-5462-8421
Fudan University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E3 ligase is widely reported to exert fundamental functions in cancers. Through rigorous bioinformatic analysis concentrating E3 ligases based on data from Genotype-Tissue Expression (GTEx) and data from The Cancer Genome Atlas (TCGA), HERC3 was indicated to be downregulated in colorectal cancer (CRC) and HERC3 downregulation showed poor overall survival (OS) and disease-free survival (DFS). Through qRT-PCR, western blotting and Immunohistochemistry (IHC), analytical results were validated based on tissues in Zhongshan hospital. Functionally, HERC3 was indicated to inhibit the migration, invasion and metastasis in vitro and in vivo through transwell assays, wound healing assays and vivo experiments. And HERC3 could regulate epithelial-mesenchymal transition (EMT) in CRC. Furthermore, immunoprecipitation (IP), coimmunoprecipitation (co-IP) and GST-pulldown assays indicated that HERC3 could directly interact with EIF5A2 in vitro and in vivo through the RCC1 domain in HERC3. And HERC3 could function as an E3 to promote the K27 and K48-linked ubiquitination degradation of EIF5A2 via the HECT domain in HERC3, besides, K47, K67, K85, and K121 in EIF5A2 were identified as ubiquitination sites. In addition, HERC3 was indicated to affect the migration, invasion and metastasis and further regulatE EMT via EIF5A2/TGF-/Smad2/3 signal. The present study may provide insight into the mechanism of EMT in CRC.

Indexed as

Colorectal NeoplasmsEpithelial-Mesenchymal TransitionPeptide Initiation FactorsRNA-Binding ProteinsUbiquitin-Protein LigasesCell Line, TumorCell MovementEukaryotic Translation Initiation Factor 5AHumansNeoplasm MetastasisUbiquitinationEukaryotic Translation Initiation Factor 5AHERC3 protein, humanPeptide Initiation FactorsRNA-Binding ProteinsUbiquitin-Protein Ligases

Identifiers

PMID35064108
PMCPMC8782983
OpenAlexW4206232440

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.