Evidence map›Paper›PMID 28373751›Full record

ArticleChinese journal of cancer research = Chung-kuo yen cheng yen chiu2017

MAGI1 inhibits migration and invasion via blocking MAPK/ERK signaling pathway in gastric cancer.

Shuqin Jia, Jiajia Lu, Tingting Qu, Yi Feng, Xiaohong Wang, Caixia Liu, Jiafu Ji

Open access · greenAbstract read
In one paragraph

Article in Chinese journal of cancer research = Chung-kuo yen cheng yen chiu, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  4. Killer cell lectin-like receptor G2 facilitates aggressive phenotypes of gastric cancer cells via dual activation of the ERK1/2 and JAK/STAT pathways.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024
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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.

Shuqin JiaLaboratory of Surgery, the Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, China; Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Center for Molecular Diagnosis, Peking University Cancer Hospital & Institute, Beijing 100142, China.
Jiajia LuDepartment of Medical Oncology, the Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, China.
Tingting QuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Center for Molecular Diagnosis, Peking University Cancer Hospital & Institute, Beijing 100142, China.
Yi FengKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Center for Molecular Diagnosis, Peking University Cancer Hospital & Institute, Beijing 100142, China.
Xiaohong WangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Tissue Bank, Peking University Cancer Hospital & Institute, Beijing 100142, China.
Caixia LiuDepartment of Medical Oncology, the Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, China.
Jiafu JiKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Gastrointestinal Surgery, Peking University Cancer Hospital & Institute, Beijing 100142, China.
Inner Mongolia Medical University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the association of membrane-associated guanylate kinase inverted 1 (MAGI1) with gastric cancer (GC) and the related molecular mechanisms.

methodsThe reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) were utilized to measure the MAGI1 expression level in GC tissues. Quantitative real-time PCR and Western blotting were used to ensure the MAGI1 expression in GC cell lines. Small hairpin RNA (shRNA) was applied for knockdown of endogenous MAGI1 in GC cells. MTT assay and colony formation assay, scratch wounding migration assay and transwell chamber migration assay, as well as transwell chamber invasion assay were employed respectively to investigate the GC cell proliferation, migration and invasion in MAGI1-knockdown and control GC cells. The potential molecular mechanism mediated by MAGI1 was studied using Western blotting and RT- PCR.

resultsRT-PCR and IHC verified MAGI1 was frequently expressed in matched adjacent noncancerous mucosa compared with GC tissues and the expression of MAGI1 was related to clinical pathological parameters. Functional assays indicated that MAGI1 knockdown significantly promoted GC cell migration and invasion. Further mechanism investigation demonstrated that one pathway of MAGI1 inhibiting migration and invasion was mainly by altering the expression of matrix metalloproteinases (MMPs) and epithelial-mesenchymal transition (EMT)-related molecules via inhibiting MAPK/ERK signaling pathway.

conclusionsMAGI1 was associated with GC clinical pathological parameters and acted as a tumor suppressor via inhibiting of MAPK/ERK signaling pathway in GC.

Indexed as

EMTgastric cancerinvasionMAGI1MAPK/ERKmigrationMMPs

Identifiers

PMID28373751
PMCPMC5348473
OpenAlexW2592982332

What OpenQuestion holds

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Read underepoch 390

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.