Evidence map›Paper›PMID 30814514›Full record

ArticleCell death & disease2019

Sortilin promotes glioblastoma invasion and mesenchymal transition through GSK-3β/β-catenin/twist pathway.

Wei Yang, Peng-Fei Wu, Jian-Xing Ma, Mao-Jun Liao, Xu-Hui Wang, Lun-Shan Xu, Min-Hui Xu, Liang Yi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.4field-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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Nerve growth factor receptor (NGFR): A key player in glioblastoma progression.Biochimica et biophysica acta. Reviews on cancer · 2026
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  11. Neurotensin modulates ovarian vascular permeability via adherens junctions.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
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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.

Wei YangDepartment of Neurosurgery, Daping Hospital and Institute Research of Surgery, Army Medical University, Chongqing, 400042, China.
Peng-Fei WuDepartment of Neurosurgery, Daping Hospital and Institute Research of Surgery, Army Medical University, Chongqing, 400042, China.
Jian-Xing MaDepartment of Neurosurgery, Daping Hospital and Institute Research of Surgery, Army Medical University, Chongqing, 400042, China.
Mao-Jun LiaoDepartment of Neurosurgery, Daping Hospital and Institute Research of Surgery, Army Medical University, Chongqing, 400042, China.
Xu-Hui WangDepartment of Neurosurgery, Daping Hospital and Institute Research of Surgery, Army Medical University, Chongqing, 400042, China.
Lun-Shan XuDepartment of Neurosurgery, Daping Hospital and Institute Research of Surgery, Army Medical University, Chongqing, 400042, China.
Min-Hui XuDepartment of Neurosurgery, Daping Hospital and Institute Research of Surgery, Army Medical University, Chongqing, 400042, China. minhuixu66@aliyun.com.
Liang YiDepartment of Neurosurgery, Daping Hospital and Institute Research of Surgery, Army Medical University, Chongqing, 400042, China. yiliangcq@126.com.
Daping Hospital · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High aggressiveness is a hallmark of glioblastoma and predicts poor prognosis of patients with glioblastoma. The expression level of sortilin has been preliminarily reported to be elevated in high-grade glioma; however, the potential significance of sortilin in glioblastoma progression has not been elucidated. In this study, we investigated the oncogenic effect of sortilin in glioblastoma. Increased levels of sortilin were noted in the mesenchymal subtype of glioblastoma and highly aggressive subtypes of glioblastoma tissues and cell lines. In addition, high levels of sortilin predicted poor prognoses in patients with glioblastoma. Sortilin knockdown or inhibition with AF38469 (an orally bioavailable inhibitor of sortilin) significantly suppressed migration and invasion by inhibiting EMT-like mesenchymal transition in glioblastoma cells. Furthermore, we proved that sortilin promoted cell invasion mainly via Glycogen synthase kinase 3 beta (GSK-3β)/β-catenin/Twist-induced EMT-like mesenchymal transition in glioblastoma. Taken together, our results demonstrate a critical role of sortilin in glioblastoma invasion and EMT-like mesenchymal transition, indicating that sortilin contributes to glioblastoma progression. These data also highlight the dramatic antitumor effects of AF38469 in glioblastoma, suggesting that AF38469 is a potentially powerful antitumor agent for sortilin-overexpressing human glioblastoma.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsbeta CateninCell Line, TumorEpithelial-Mesenchymal TransitionGlioblastomaGlycogen Synthase Kinase 3 betaHumansMiceMice, NudeSortilinTransfectionAdaptor Proteins, Vesicular Transportbeta CateninGlycogen Synthase Kinase 3 betaSortilin

Identifiers

PMID30814514
PMCPMC6393543
OpenAlexW2915909596

What OpenQuestion 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 OpenQuestion graph.