Evidence map›Paper›PMID 38881325›Full record

ArticleCancer medicine2024

TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation.

Fei Wu, Jiaqi Xu, Xin Jin, Yue Zhu, Wenxin Gao, Meng Liu, Yan Zhang, Weifeng Qian, Xiaoyan Huang, Dan Zhao and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer medicine, 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. VDAC2: an emerging pivotal and multifaceted regulator in tumor biology.Apoptosis : an international journal on programmed cell death · 2026
    Review
  4. Article
  5. Article
  6. Multifaceted role ofMedComm · 2024
    Review
  7. 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

13 authors.

Fei WuDepartment of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.
Jiaqi XuDepartment of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.
Xin JinDepartment of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.
Yue ZhuDepartment of Breast and Thyroid Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.
Wenxin GaoDepartment of Histology and Embryology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Meng LiuDepartment of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.
Yan ZhangDepartment of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.
Weifeng QianDepartment of Breast and Thyroid Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.ORCID 0000-0001-8175-0513
Xiaoyan HuangDepartment of Histology and Embryology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Dan ZhaoReproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Guannan FengDepartment of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.
Shunyu HouDepartment of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.
Xiaoxue XiDepartment of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.ORCID 0000-0002-0549-5589

Funding

Cultivation Special Project of Gusu School of Nanjing Medical University GSKY20220522Key Research Foundation of Zhenjiang Social Development SH2022029"Science and Education Revitalize Health" Youth Science and Technology Project of Suzhou KJXW2020028Science and Technology Project of Suzhou of Jiangsu Province SYS2020175Scientific Research Project of Gusu School of Nanjing Medical University GSKY20210203Scientific Research Project of Gusu School of Nanjing Medical University GSKY20210208Special project of diagnosis and treatment technology for key clinical diseases of Suzhou of Jiangsu Province LCZX202013
6 · The paper itself

Abstract

backgroundOvarian cancer is a common gynecological tumor with high malignant potential and poor prognosis. TRIM8, is involved in the development of various tumors, but its precise regulatory role in ovarian cancer is still unknown.

aimsThe aim of this study was to explore the specific mechanism by which TRIM8 regulates ovarian cancer. MATERIALS AND

methodsWe used bioinformatics analysis to screen for high expression of TRIM8 in ovarian cancer. The expression of TRIM8 in healthy and cancerous ovarian tissues was assessed by immunofluorescence. TRIM8 was silenced or overexpressed in ovarian cancer cell lines, with cell proliferation and migration evaluated by CCK8, transwell and clonal formation assays. The effect of TRIM8 on ovarian cancer cells in vivo was assessed by subcutaneous tumor formation experiments in nude mice. The potential interacting protein VDAC2 was identified by mass spectrometry. The mechanism underlying TRIM8 regulation of VDAC2 was evaluated by co-immunoprecipitation and western blotting.

resultsTRIM8 was overexpressed in ovarian cancer. TRIM8 promoted the proliferation and migration of ovarian cancer cells in vitro and the growth of subcutaneous tumors in mice in vivo. TRIM8 interacted with VDAC2, weakened the stability of the protein, and promoted its polyubiquitination and subsequent degradation. Knockdown of VDAC2 increased the resistance of ovarian cancer cells to iron death, whereas overexpression of VDAC2 attenuated ovarian cancer progression induced by TRIM8 overexpression. DISCUSSION: TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation, these finding may provide new targets for the treatment of ovarian cancer.

conclusionTRIM8 degraded VDAC2 through the ubiquitination pathway, increased the resistance of ovarian cancer cells to iron death, and promoted the proliferation and migration of ovarian cancer.

Indexed as

Cell MovementOvarian NeoplasmsProteolysisUbiquitinationVoltage-Dependent Anion Channel 2AnimalsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeXenograft Model Antitumor AssaysVDAC2 protein, humanVoltage-Dependent Anion Channel 2E3 ubiquitin ligaseovarian cancerTRIM8VDAC2

Identifiers

PMID38881325
PMCPMC11180974

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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.