Evidence map›Paper›PMID 37539927›Full record

ArticleCurrent cancer drug targets2024

SULF1 Activates the VEGFR2/PI3K/AKT Pathway to Promote the Development of Cervical Cancer.

Juan Li, Xihao Wang, Zhilong Li, Minzhen Li, Xuelian Zheng, Danxi Zheng, Yanyun Wang, Mingrong Xi

Abstract read
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In one paragraph

Article in Current cancer drug targets, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed, 9 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

8 authors at 2 institutions in 1 country.

Juan LiDepartment of Gynecology and Obstetrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Xihao WangDepartment of Pathology, Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 611731, China.
Zhilong LiLaboratory of Molecular Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Minzhen LiDepartment of Gynecology and Obstetrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Xuelian ZhengDepartment of Gynecology and Obstetrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Danxi ZhengDepartment of Gynecology and Obstetrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Yanyun WangLaboratory of Molecular Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Mingrong XiDepartment of Gynecology and Obstetrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Sichuan University · CNUniversity of Electronic Science and Technology of China · CN

Funding

Chengdu Municipal Health Commission 2021146Key Research and Development projects of Sichuan Province 2020YFS0129National Natural Science Foundation of China 61875249
6 · The paper itself

Abstract

background and purposeSulfatase 1 (SULF1) can regulate the binding of numerous signaling molecules by removing 6-O-sulfate from heparan sulfate proteoglycans (HSPGs) to affect numerous physiological and pathological processes. Our research aimed to investigate the effect of the SULF1-mediated VEGFR2/PI3K/AKT signaling pathway on tumorigenesis and development of cervical cancer (CC).

methodsThe expression and prognostic values of SULF1 in patients with CC were analyzed through bioinformatics analysis, qRT-PCR, immunohistochemistry, and western blot. The function and regulatory mechanism of SULF1 in proliferation, migration, and invasion of cervical cancer cells were examined through lentivirus transduction, CCK8, flow cytometry analysis, plate colony formation assay, scratch assay, transwell assay, western blot, VEGFR2 inhibitor (Ki8751), and mouse models.

resultsSULF1 expression was significantly upregulated in CC tissues, which was significantly associated with poor prognosis of patients with CC.

conclusionSULF1 plays an oncogenic role in the tumorigenesis and development of CC, indicating its potential as a novel molecular target for gene-targeted therapy in patients with CC.

Indexed as

Cell ProliferationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionSulfotransferasesUterine Cervical NeoplasmsVascular Endothelial Growth Factor Receptor-2AnimalsApoptosisCell MovementFemaleGene Expression Regulation, NeoplasticHeLa CellsHumansMiceMice, Inbred BALB CKDR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSULF1 protein, humanSulfotransferasesVascular Endothelial Growth Factor Receptor-2cervical cancerHeLa cellsheparan sulfate proteoglycans.Ki8751SULF1VEGFR2

Identifiers

PMID37539927
OpenAlexW4385564435

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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.