Evidence map›Paper›PMID 33328743›Full record

ArticleOncoTargets and therapy2020

MAGOH/MAGOHB Inhibits the Tumorigenesis of Gastric Cancer via Inactivation of b-RAF/MEK/ERK Signaling.

Yong Zhou, Zhongqi Li, Xuan Wu, Laizhen Tou, Jingjing Zheng, Donghui Zhou

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 47 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 2 institutions in 1 country.

Yong Zhou *Department of Oncology, First Affiliated Hospital,  Zhejiang University School of Medicine, Hangzhou 310003, People's Republic of China.
Zhongqi Li *Department of Oncology, First Affiliated Hospital,  Zhejiang University School of Medicine, Hangzhou 310003, People's Republic of China.
Xuan WuDepartment of Oncology, First Affiliated Hospital,  Zhejiang University School of Medicine, Hangzhou 310003, People's Republic of China.
Laizhen TouDepartment of Oncology, First Affiliated Hospital,  Zhejiang University School of Medicine, Hangzhou 310003, People's Republic of China.
Jingjing ZhengDepartment of General Surgery, Lishui Municipal Central Hospital, Lishui, Zhejiang 323000, People's Republic of China.
Donghui ZhouDepartment of Oncology, First Affiliated Hospital,  Zhejiang University School of Medicine, Hangzhou 310003, People's Republic of China.
First Affiliated Hospital Zhejiang University · CNLishui Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGastric cancer is one of the most malignant tumors all over the world. It has been reported that proteins play key roles during the tumorigenesis of gastric cancer. To identify novel potential targets for gastric cancer, differential expressed proteins between gastric cancer and adjacent normal tissues were analyzed with proteomics and bioinformatics tool.

methodsThe differentially expressed proteins between gastric cancer and adjacent normal tissues were analyzed by Omicsbean (multi-omics data analysis tool). Cell viability was tested by CCK-8 assay. Flow cytometry was used to measure cell apoptosis and cycle. Transwell assay was used to test cell migration and invasion. Gene and protein expressions were detected by RT-qPCR, immunohistochemistry and Western blot, respectively.

resultsMAGOH and MAGOHB were found to be notably upregulated in gastric cancer tissues compared with that in normal tissues. Knockdown of MAGOH significantly inhibited the proliferation of gastric cancer cells via inducing the cell apoptosis. In addition, MAGOH knockdown induced G2 phase arrest in gastric cancer cells. Moreover, MAGOH knockdown notably inhibited migration and invasion of gastric cancer cells. Importantly, double knockdown of MAGOH and MAGOHB exhibited much better anti-tumor effects on gastric cancer compared with alone treatment. Finally, double knockdown of MAGOH and MAGOHB mediated the tumorigenesis of gastric cancer via regulation of RAF/MEK/ERK signaling.

conclusionMAGOH knockdown inhibited the tumorigenesis of gastric cancer via mediation of b-RAF/MEK/ERK signaling, and double knockdown of MAGOH and MAGOHB exhibited much better anti-tumor effects. This finding might provide us a new strategy for the treatment of gastric cancer.

Indexed as

b-RAF/MEK/ERK signalinggastric cancerMAGOH/MAGOHB

Identifiers

PMID33328743
PMCPMC7735944
OpenAlexW3111084272

What Socratic 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 Socratic graph.