Evidence map›Paper›PMID 32314457›Full record

ArticleCancer science2020

Downregulation of α-l-fucosidase 1 suppresses glioma progression by enhancing autophagy and inhibiting macrophage infiltration.

Lixia Xu, Zhenwei Li, Sirong Song, Qian Chen, Lidong Mo, Chen Wang, Weijia Fan, Yan Yan, Xiaoguang Tong, Hua Yan

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

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  20. Macrophages/Microglia in the Glioblastoma Tumor Microenvironment.International journal of molecular sciences · 2021
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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

10 authors at 2 institutions in 1 country.

Lixia XuTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, China.
Zhenwei LiDepartment of Neurosurgery, Tianjin Huanhu Hospital, Tianjin, China.
Sirong SongGraduate School of Tianjin Medical University, Tianjin, China.
Qian ChenGraduate School of Tianjin Medical University, Tianjin, China.
Lidong MoTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, China.
Chen WangTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, China.
Weijia FanTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, China.
Yan YanClinical Laboratory, Tianjin Huanhu Hospital, Tianjin, China.
Xiaoguang TongTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, China.
Hua YanTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, China.ORCID https://orcid.org/0000-0003-3482-0261
Tianjin Huanhu Hospital · CNTianjin Medical University · CN

Funding

National Natural Science Foundation of China 81972349Tianjin Municipal Science and Technology Commission 16JCQNJC10200
6 · The paper itself

Abstract

α-l-Fucosidase 1 (FUCA1), a lysosomal enzyme that catalyses the hydrolytic cleavage of the terminal fucose residue, has been reported to be involved in tumorigenesis. However, the clinical significance and biological roles of FUCA1 in glioma remain largely unknown. We analyzed FUCA1 expression according to data in Oncomine, The Cancer Genome Atlas, and Chinese Glioma Genome Atlas databases and further verified FUCA1 expression with immunohistochemistry and real-time PCR analysis in glioma tissues. The results showed that FUCA1 overexpression was significantly associated with high-grade glioma as well as high mortality rates in the survival analysis. Data analyzed in cBioPortal showed that alterations in FUCA1 (1.4%) were correlated with worse survival in glioblastoma multiforme patients. Functional experiments showed that downregulation of FUCA1 suppressed glioma growth in vitro and in vivo. Conversely, overexpression of FUCA1 had the opposite effects on glioma. Mechanistically, transient inhibition of FUCA1 promoted the formation of large acidic vacuoles, as revealed by staining with acridine orange, increased the ratio of LC3-B/LC3-A, and modified the expression of Beclin-1 and Atg12, which are autophagic markers. Upregulation of FUCA1 attenuated starvation-induced autophagy in glioma. In addition, lower levels of tumor-infiltrating macrophages, including CD68

Indexed as

Gene Expression Regulation, Neoplasticalpha-L-FucosidaseAnimalsAutophagyCell Line, TumorDisease Models, AnimalGene Expression ProfilingGliomaHumansImmunohistochemistryMacrophagesMiceMutationPrognosisTumor MicroenvironmentXenograft Model Antitumor Assaysalpha-L-Fucosidaseautophagygliomamacrophageprognosisα-l-fucosidase 1

Identifiers

PMID32314457
PMCPMC7385365
OpenAlexW3016287558

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.