Evidence map›Paper›PMID 36829196›Full record

ArticleJournal of ovarian research2023

Molecular mechanism of Wilms' tumor (Wt1) (+/-KTS) variants promoting proliferation and migration of ovarian epithelial cells by bioinformatics analysis.

Xiaomei Wang, Jingyu Zhao, Yixin Zhang, Yuxin Liu, Jinzheng Wang, Ruoxi Shi, Jinxiang Yuan, Kai Meng

Open access · goldAbstract read
In one paragraph

Article in Journal of ovarian research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

8 authors at 1 institution in 1 country.

Xiaomei WangCollege of Basic Medicine, Jining Medical University, Jining, China.
Jingyu ZhaoCollaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining Medical University, Jining, China.
Yixin ZhangCollaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining Medical University, Jining, China.
Yuxin LiuCollaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining Medical University, Jining, China.
Jinzheng WangCollaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining Medical University, Jining, China.
Ruoxi ShiCollaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining Medical University, Jining, China.
Jinxiang YuanCollaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining Medical University, Jining, China. yuanjinxiang18@163.com.
Kai MengCollaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining Medical University, Jining, China. mengkai521888@126.com.
Jining Medical University · CN

Funding

College Students' Innovation Training Program of Jining Medical University cx2021038Research Fund for Lin He's Academician Workstation of New Medicine and Clinical Translation in Jining Medical University JYHL2021MS13Research Startup Fund of Jining Medical University 600791001Shandong Provincial Natural Science Foundation ZR2020QH042Shandong Provincial Natural Science Foundation ZR2022QC188
6 · The paper itself

Abstract

Epithelial ovarian cancer (EOC) is a gynecological disease with the highest mortality. With the lack of understanding of its pathogenesis, no accurate early diagnosis and screening method has been established for EOC. Studies revealed the multi-faceted function of Wilms' tumor (Wt1) genes in cancer, which may be related to the existence of multiple alternative splices. Our results show that Wt1 (+KTS) or Wt1 (-KTS) overexpression can significantly promote the proliferation and migration of human ovarian epithelial cells HOSEpiC, and Wt1 (+KTS) effects were more evident. To explore the Wt1 (+/-KTS) variant mechanism in HOSEpiC proliferation and migration and ovarian cancer (OC) occurrence and development, this study explored the differential regulation of Wt1 (+/-KTS) in HOSEpiC proliferation and migration by transcriptome sequencing. OC-related hub genes were screened by bioinformatics analysis to further explore the differential molecular mechanism of Wt1 (+/-KTS) in the occurrence of OC. Finally, we found that the regulation of Wt1 (+/-KTS) variants on the proliferation and migration of HOSEpiC may act through different genes and signaling pathways and screened out key genes and differentially regulated genes that regulate the malignant transformation of ovarian epithelial cells. The implementation of this study will provide new clues for the early diagnosis and precise treatment of OC.

Indexed as

Kidney NeoplasmsWilms TumorCell ProliferationComputational BiologyEpithelial CellsHumansWT1 ProteinsWT1 protein, humanWT1 ProteinsBioinformatics analysisMigrationOvarian epithelial cellsProliferationWilms’ tumor (Wt1) (+/−KTS)

Identifiers

PMID36829196
PMCPMC9951437
OpenAlexW4321787361

What Socratic 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 Socratic graph.