Evidence map›Paper›PMID 35130130›Full record

ArticleCell cycle (Georgetown, Tex.)2022

UBE2T is upregulated, predicts poor prognosis, and promotes cell proliferation and invasion by promoting epithelial-mesenchymal transition via inhibiting autophagy in an AKT/mTOR dependent manner in ovarian cancer.

Wei Huang, Hongyan Huang, Yuzhen Xiao, Lei Wang, Tingting Zhang, Xiaoling Fang, Xiaomeng Xia

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Autophagy in Ovarian Cancer, an Opportunity or an Additional Threat?International journal of molecular sciences · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Silencing ofOncology letters · 2023
    Article
  11. Role of autophagy and its regulation by noncoding RNAs in ovarian cancer.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  12. Article
  13. Review
  14. Article
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 1 institution in 1 country.

Wei HuangDepartment of Otolaryngology Head and Neck Surgery, Xiangya Hospital, Central South University, Changsha, China.
Hongyan HuangDepartment of Obstetrics and Gynecology, The Second Xiangya Hospital, Central South University, Changsha, P.R. China.
Yuzhen XiaoDepartment of Obstetrics and Gynecology, The Second Xiangya Hospital, Central South University, Changsha, P.R. China.
Lei WangNhc Key Laboratory of Carcinogenesis, Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha, China.
Tingting ZhangDepartment of Obstetrics and Gynecology, The Second Xiangya Hospital, Central South University, Changsha, P.R. China.
Xiaoling FangDepartment of Obstetrics and Gynecology, The Second Xiangya Hospital, Central South University, Changsha, P.R. China.ORCID 0000-0001-6005-9598
Xiaomeng XiaDepartment of Obstetrics and Gynecology, The Second Xiangya Hospital, Central South University, Changsha, P.R. China.ORCID 0000-0002-2647-2925
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant upregulation and oncogenic roles of UBE2T are revealed in several cancers. However, the expression, clinical significance, and functions of UBE2T have not been explored in ovarian cancer (OC). In this study, the expression of UBE2T and its relation with clinicopathological features and prognosis of OC patients were explored by analyzing online data and experimental data. Besides, the functions of UBE2T in OC cells were investigated by in vitro experiments, including CCK-8, plate clone formation, and Transwell assays. Finally, the underlying mechanism of UBE2T associated functions in OC was analyzed. The results indicated that UBE2T was significantly upregulated in OC tissues. UBE2T expression was notably correlated with clinical features, such as primary T stage and FIGO stage in OC patients. UBE2T, acting as an independent prognostic indicator, was inversely associated with the prognosis of OC patients. The UBE2T knockdown remarkably suppressed the growth, proliferation, and invasion of OC cells, indicated by impaired cell viability, fewer cell clones, and invasive cells. Mechanistically, UBE2T depletion suppressed epithelial-mesenchymal transition (EMT), which was caused by autophagy activation due to inactivation of AKT/mTOR in OC cells with UBE2T knockdown. Collectively, our findings confirm that UBE2T upregulation predicts poor prognosis and promotes malignant progression in OC. UBE2T upregulation suppresses autophagy and subsequently boosts EMT via activating the AKT/mTOR axis, which accounts for the underlying mechanism of oncogenic roles of UBE2T in OC.

Indexed as

Ovarian NeoplasmsProto-Oncogene Proteins c-aktAutophagyCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionFemaleHumansTOR Serine-Threonine KinasesUbiquitin-Conjugating EnzymesMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesUBE2T protein, humanUbiquitin-Conjugating EnzymesAKT/mTORautophagyepithelial–mesenchymal transition (EMT)Ovarian cancerubiquitin-conjugating enzyme E2T (UBE2T)

Identifiers

PMID35130130
PMCPMC8973388
OpenAlexW4210409719

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.