Evidence map›Paper›PMID 32319576›Full record

ArticleInternational journal of oncology2020

HECTD1 regulates the expression of SNAIL: Implications for epithelial‑mesenchymal transition.

Xinggang Wang, Christian De Geyter, Zanhui Jia, Ya Peng, Hong Zhang

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025
    Review
  3. Review
  4. Article
  5. 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

5 authors at 2 institutions in 2 countries.

Xinggang WangDepartment of Biomedicine (DBM), University Hospital, University of Basel, CH‑4031 Basel, Switzerland.
Christian De GeyterDepartment of Biomedicine (DBM), University Hospital, University of Basel, CH‑4031 Basel, Switzerland.
Zanhui JiaSecond Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.
Ya PengDepartment of Biomedicine (DBM), University Hospital, University of Basel, CH‑4031 Basel, Switzerland.
Hong ZhangDepartment of Biomedicine (DBM), University Hospital, University of Basel, CH‑4031 Basel, Switzerland.
University Hospital of Basel · CHSecond Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a transcription factor, SNAIL plays a crucial role in embryonic development and cancer progression by mediating epithelial‑mesenchymal transition (EMT); however, post‑translational modifications, such as ubiquitination, which control the degradation of SNAIL have been observed to affect its functional role in EMT. In a previous study by the authors, it was demonstrated that the HECT domain E3 ubiquitin ligase 1 (HECTD1) regulated the dynamic nature of adhesive structures. In the present study, HECTD1 was observed to interact with SNAIL and regulate its stability through ubiquitination, and the knockdown of HECTD1 increased the expression levels of SNAIL. HECTD1 was discovered to contain putative nuclear localization and export signals that facilitated its translocation between the cytoplasm and nucleus, a process regulated by epidermal growth factor (EGF). Treatment with leptomycin B resulted in the nuclear retention of HECTD1, which was associated with the loss of SNAIL expression. The knockdown of HECTD1 in HeLa cells increased cell migration and induced a mesenchymal phenotype, in addition to demonstrating sustained EGF signaling, which was observed through increased phosphorylated ERK expression levels. Under hypoxic conditions, HECTD1 expression levels were decreased by microRNA (miRNA or miR)‑210. Upon the observation of genetic abnormalities in the HECTD1 gene in cervical cancer specimens, it was observed that the decreased expression levels of HECTD1 were significantly associated with a poor patient survival. Thus, it was hypothesized that HECTD1 may regulate EMT through the hypoxia/hypoxia inducible factor 1α/miR‑210/HECTD1/SNAIL signaling pathway and the EGF/EGF receptor/HECTD1/ERK/SNAIL signaling pathway in cervical cancer. On the whole, the data of the present study indicated that HECTD1 serves as an E3 ubiquitin ligase to mediate the stability of SNAIL proteins.

Indexed as

Cell MovementDown-RegulationEpidermal Growth FactorEpithelial-Mesenchymal TransitionFatty Acids, UnsaturatedFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeLa CellsHumansNuclear Export SignalsNuclear Localization SignalsProtein StabilityProtein TransportSnail Family Transcription FactorsUbiquitinationEpidermal Growth FactorFatty Acids, UnsaturatedHECTD1 protein, humanleptomycin BNuclear Export SignalsNuclear Localization SignalsSnail Family Transcription FactorsUbiquitin-Protein Ligasescervical cancerepidermal growth factor receptor signalingepithelial-mesenchymal transitionHECT domain E3 ubiquitin ligase 1nuclear localizationSNAIL

Identifiers

PMID32319576
PMCPMC7115742
OpenAlexW3007741793

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.