Evidence map›Paper›PMID 27178818›Full record

ArticleOncology research2016

Overexpression of SASH1 Inhibits TGF-β1-Induced EMT in Gastric Cancer Cells.

Wei Zong, Chen Yu, Ping Wang, Lei Dong

Open access · hybridAbstract read
In one paragraph

Article in Oncology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  12. Fusobacterium nucleatum produces cancer stem cell characteristics via EMT-resembling variations.International journal of clinical and experimental pathology · 2020
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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

4 authors at 1 institution in 1 country.

Wei ZongDepartment of Gastroenterology, Shaanxi Provincial People's Hospital, the Third Affiliated Hospital, College of Medicine, Xi'an Jiaotong University, Xi'an, China.
Chen Yu
Ping Wang
Lei Dong
Shaanxi Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epithelial-mesenchymal transition (EMT) is considered to be one of the critical steps in gastric cancer cell invasion and metastasis. SAM- and SH3-domain containing 1 (SASH1), a member of the SLY family of signal adapter proteins, is a candidate for tumor suppression in several cancers. However, the biological role of SASH1 in gastric cancer remains largely unknown. Therefore, the purpose of this study was to investigate the impact of SASH1 on the biological behavior of gastric cancer cells treated with transforming growth factor (TGF)-β1. In the current study, we provide evidence that SASH1 was lowly expressed in human gastric cancer cells, and TGF-β1 also inhibited the expression of SASH1 in TSGH cells. We found that SASH1 inhibited TGF-β1-mediated EMT in TSGH cells, as well as cell migration and invasion. Furthermore, SASH1 obviously inhibited the phosphorylation of PI3K and Akt in TGF-β1-stimulated TSGH cells. In summary, our study is the first to show that overexpression of SASH1 inhibits TGF-β1-induced EMT in gastric cancer cells through the PI3K/Akt signaling pathway. These results suggest that SASH1 may be a potential therapeutic target for the treatment of gastric cancer.

Indexed as

Cell Line, TumorCell MovementEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionStomach NeoplasmsTransforming Growth Factor beta1Tumor Suppressor ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSASH1 protein, humanTransforming Growth Factor beta1Tumor Suppressor Proteins

Identifiers

PMID27178818
PMCPMC7838734
OpenAlexW2390584831

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.