Evidence map›Paper›PMID 35393406›Full record

ArticleCell death discovery2022

MOXD1 knockdown suppresses the proliferation and tumor growth of glioblastoma cells via ER stress-inducing apoptosis.

Pengfei Shi, Jie Xu, Fanwei Xia, Yinggang Wang, Jie Ren, Ping Liang, Hongjuan Cui

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  9. Science advances · 2024
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  14. Exome Sequencing in an ADSHE Family: VUS Identification and Limits.International journal of environmental research and public health · 2022
    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

7 authors at 2 institutions in 1 country.

Pengfei ShiState Key Laboratory of Silkworm Genome Biology, Southwest University, 400716, Chongqing, China.
Jie XuState Key Laboratory of Silkworm Genome Biology, Southwest University, 400716, Chongqing, China.
Fanwei XiaState Key Laboratory of Silkworm Genome Biology, Southwest University, 400716, Chongqing, China.
Yinggang WangCancer Center, Medical Research Institute, Southwest University, 400716, Chongqing, China.
Jie RenCancer Center, Medical Research Institute, Southwest University, 400716, Chongqing, China.
Ping LiangDepartment of Neurosurgery, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, 400014, China. liangping868@sina.com.
Hongjuan CuiState Key Laboratory of Silkworm Genome Biology, Southwest University, 400716, Chongqing, China. hcui@swu.edu.cn.ORCID http://orcid.org/0000-0003-1178-1570
Southwest University · CNChildren's Hospital of Chongqing Medical University · CN

Funding

Natural Science Foundation of Chongqing (Natural Science Foundation of Chongqing Municipality) cstc2019jcyjzdxmX0033
6 · The paper itself

Abstract

Oxygenase-catalyzed reduction and activation of oxygen molecules and the incorporation of oxygen atoms into organic molecules are undoubtedly necessary in the process of tumor development, and it is also one of the research hotspots in recent years. MOXD1 belongs to the copper-dependent monooxygenase family. The expression of MOXD1 is one of the characteristics of early tumor development. However, it is not understandable that the biological function and molecular mechanism of MOXD1 in Glioblastoma (GBM). In this study, high MOXD1 expression is strongly associated with poor survival of the patient with GBM. Moreover. MOXD1 knockdown can inhibit cell viability, proliferation, migration, invasion, and tumorigenesis of GBM cells. This is also proven for the first time that MOXD1 can bind to β3GnT2 and affect the glycosylation modification of some proteins. In addition, knockdown of MOXD1 induces endoplasmic reticulum (ER) stress and triggers the ER-mitochondrial apoptosis pathway. Taken together, these results reveal that MOXD1 is involved in the occurrence and development of GBM, and also provide a new strategy for targeted therapy.

Identifiers

PMID35393406
PMCPMC8991257
OpenAlexW4224309282

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.