Evidence map›Paper›PMID 23661031›Full record

ArticleDigestive diseases and sciences2013

Semaphorin 5A promotes gastric cancer invasion/metastasis via urokinase-type plasminogen activator/phosphoinositide 3-kinase/protein kinase B.

Guoqing Pan, Zhu Zhu, Jian Huang, Chenggang Yang, Ying Yang, Yingxia Wang, Xiaoyu Tuo, Guomiao Su, Xiangling Zhang, Zhi Yang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Digestive diseases and sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

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  14. Loss of plexin-B3 in hepatocellular carcinoma.Experimental and therapeutic medicine · 2015
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  15. SEMA4b inhibits MMP9 to prevent metastasis of non-small cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
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

11 authors at 3 institutions in 1 country.

Guoqing PanDepartment of Pathology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, People's Republic of China.
Zhu Zhu
Jian Huang
Chenggang Yang
Ying Yang
Yingxia Wang
Xiaoyu Tuo
Guomiao Su
Xiangling Zhang
Zhi Yang
Tao Liu
Kunming Medical University · CNFirst Affiliated Hospital of Kunming Medical University · CNFirst People's Hospital of Yunnan Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSemaphorin 5A, a member of the semaphorin family, was originally identified as an axonal guidance factor functioning during neuronal development. Previously, we showed that the expression of semaphorin 5A might contribute to the metastasis of gastric cancer. However, less information is currently available as to the involvement of uPA in the semaphorin 5A-induced metastasis and invasion of gastric cancer cells.

aimThe present study was designed to test whether semaphorin 5A mediates the invasion and metastasis of gastric cancer via PI3K/Akt/uPA signaling.

methodsThe semaphorin 5A-overexpressing cell was established from the gastric cancer cell line AGS. The effect of semaphorin 5A on the expression of uPA was evaluated by ELISA and Western blotting as well as RT-PCR assays, respectively. Synthetic or natural inhibitors and dominant-negative mutants were used to determine the hierarchical relationship between semaphorin 5A, PI3K/Akt and uPA in the invasion and metastasis of gastric cancer.

resultsOverpression of semaphorin 5A enhanced the expression of uPA, and synthetic or natural inhibitors of uPA abolished semaphorin 5A-induced cell migration and invasion. Semaphorin 5A overexpression promoted the phosphorylation of Akt. Blocking effects of PI3K/Akt using pharmacologic inhibitors, dominant-negative mutants abolished the ability of semaphorin 5A to induce uPA expression and cell invasion and migration.

conclusionSemaphorin 5A could promote invasion and metastasis of gastric cancer through the PI3K/Akt/uPA signal transduction pathway. Semaphorin 5A and its regulated molecules could be the potential targets for cancer therapy.

Indexed as

AnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMembrane ProteinsMiceMice, NudeNeoplasm InvasivenessNeoplasm MetastasisNeoplasms, ExperimentalNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSemaphorinsStomach NeoplasmsMembrane ProteinsNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSEMA5A protein, humanSemaphorinsUrokinase-Type Plasminogen Activator

Identifiers

PMID23661031
PMCPMC3731515
OpenAlexW2082970093

What OpenQuestion holds

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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.