Evidence map›Paper›PMID 38466034›Full record

ArticleCancer medicine2024

High TPX2 expression results in poor prognosis, and Sp1 mediates the coupling of the CX3CR1/CXCL10 chemokine pathway to the PI3K/Akt pathway through targeted inhibition of TPX2 in endometrial cancer.

Mei Yang, Xiaogang Mao, Lin Li, Jiang Yang, Hui Xing, Chunfan Jiang

Open access · goldAbstract 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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Mei YangDepartment of Obstetrics and Gynecology, Xiangyang Central Hospital, Affiliated Hospital of Hubei, University of Arts and Science, Xiangyang, China.
Xiaogang MaoDepartment of Obstetrics and Gynecology, Xiangyang Central Hospital, Affiliated Hospital of Hubei, University of Arts and Science, Xiangyang, China.
Lin LiDepartment of Obstetrics and Gynecology, Xiangyang Central Hospital, Affiliated Hospital of Hubei, University of Arts and Science, Xiangyang, China.
Jiang YangDepartment of Obstetrics and Gynecology, Xiangyang Central Hospital, Affiliated Hospital of Hubei, University of Arts and Science, Xiangyang, China.
Hui XingDepartment of Obstetrics and Gynecology, Xiangyang Central Hospital, Affiliated Hospital of Hubei, University of Arts and Science, Xiangyang, China.
Chunfan JiangInstitute of Maternity Disease, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China.ORCID 0000-0002-4213-5718
Hubei University of Arts and Science · CN

Funding

Foundation of Hubei University of Arts and Science XK2019046National Natural Science Foundation of China 81972449
6 · The paper itself

Abstract

introductionApproximately 30% of individuals with advanced EC have unsatisfactory prognosis. Evidence suggests that TPX2 is frequently upregulated in malignancies and related to cancer progression. Its role and pathological mechanism in EC need further research.

methodsGSEA and TPX2 expression, GO, KEGG, and prognostic analyses were performed with TCGA data by bioinformatic approaches. Relationships between TPX2 expression and clinicopathological parameters were investigated immunohistochemically and statistically. shRNA and overexpression plasmids were constructed and transfected into AN3CA and Ishikawa cells to evaluate phenotypic changes and injected into nude mouse axillae. Coimmunoprecipitation and chromatin immunoprecipitation were used to identify interacting proteins and promoter-binding sequences. Changes in TPX2 expression were identified by Western blotting and RT-qPCR.

resultsTPX2 expression was significantly higher in EC tissues than in normal tissues in TCGA and in-house specimens (all p < 0.001). In survival analysis, high TPX2 expression was associated with poor prognosis (p = 0.003). TPX2 overexpression stimulated cancer cell proliferation, promoted the G0-G1-to-G2/M transition, enhanced invasion and migration, and accelerated tumor growth in nude mice. TPX2 regulated the CX3CR1/CXCL10 chemokine pathway and activated the PI3K/Akt signaling pathway. Sp1 negatively regulated TPX2 expression, affecting the malignant progression of endometrial cancer cells by coupling the CX3CR1/CXCL10 chemokine pathway to the PI3K/Akt signaling pathway.

conclusionTPX2 could be a prognostic biomarker for EC and play an important role in the CX3CR1/CXCL10 chemokine pathway and PI3K/Akt pathway via Sp1.

Indexed as

Chemokine CXCL10Endometrial NeoplasmsAnimalsCell Cycle ProteinsCX3C Chemokine Receptor 1FemaleHumansMiceMice, NudeMicrotubule-Associated ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCell Cycle ProteinsChemokine CXCL10CX3C Chemokine Receptor 1CX3CR1 protein, humanCXCL10 protein, humanMicrotubule-Associated ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTPX2 protein, humanCX3CR1/CXCL10 chemokine pathwayendometrial cancerPI3K/Akt signaling pathwaySp1TPX2

Identifiers

PMID38466034
PMCPMC10926884
OpenAlexW4392644795

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.