Evidence map›Paper›PMID 37432513›Full record

ArticleFunctional & integrative genomics2023

TRIP 13-dependent pathways promote the development of gastric cancer.

Fengming Ni, Xinmin Liu, Yan Xia, He Zhu, Fudong Li, Nan Zhang, Hong Xu

Open access · hybridAbstract read
In one paragraph

Article in Functional & integrative genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. 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 2 institutions in 1 country.

Fengming NiDepartment of Gastroenterology, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun, 130021, China.
Xinmin LiuDepartment of Neurology, The First Hospital of Jilin University, Changchun, China.
Yan XiaDepartment of Gastroenterology, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun, 130021, China.
He ZhuDepartment of Gastroenterology, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun, 130021, China.
Fudong LiDepartment of Gastroenterology, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun, 130021, China.
Nan ZhangDepartment of Gastroenterology, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun, 130021, China.
Hong XuDepartment of Gastroenterology, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun, 130021, China. x_hong@jlu.edu.cn.
Jilin University · CNFirst Hospital of Jilin University · CN

Funding

Department of Finance of Jilin Province JLSWSRCZX2020-006National Natural Science Foundation of China 3A417E013428
6 · The paper itself

Abstract

TRIP13 is highly expressed in various human tumors and promotes tumorigenesis. We aimed to explore the biological effect of TRIP13 on gastric cancer. The RNA sequence data were retrieved from TCGA to evaluate TRIP13 mRNA expression in gastric cancer. Paired formalin-fixed paraffin-embedded blocks were further analyzed to verify the relationship between TRIP13 expression and carcinogenic status. The functions of TRIP13 on the proliferation of gastric malignancy were investigated by MTT, flow cytometry, colony formation experiment, and nude mouse tumor formation experiment. Finally, microarray analysis of TRIP13-related pathways was performed to identify the potential underlying mechanism of TRIP13 in gastric cancer. TRIP13 was found to have high expression in tumor samples. TRIP13 expression status was significantly subjective to tumor-node-metastasis (TNM) staging and poor survival. The downregulation of TRIP13 promoted apoptosis and inhibited tumor growth. TRIP13-dependent JAK/STAT and NF-κB signaling cascade were found as two key pathways in the carcinogenesis of GC. In conclusion, TRIP13 participates in the carcinogenesis of stomach cancer, and its overexpression in the cancerous tissues dovetail with advanced stage and survival. Moreover, TRIP13 functions as an upstream regulator of the JAK/STAT and p53 signaling pathways, which play critical roles in developing various malignancies.

Indexed as

Stomach NeoplasmsAnimalsApoptosisATPases Associated with Diverse Cellular ActivitiesCarcinogenesisCell Cycle ProteinsDown-RegulationHumansMiceNF-kappa BATPases Associated with Diverse Cellular ActivitiesCell Cycle ProteinsNF-kappa BTRIP13 protein, humanGastric cancerGene set enrichment analysis (GSEA)Oncogenic pathwaysSurvival relevanceTRIP13

Identifiers

PMID37432513
PMCPMC10335954
OpenAlexW4383873072

What OpenQuestion holds

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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.