Evidence map›Paper›PMID 29367342›Full record

ArticleThe Journal of biological chemistry2018

GSE1 predicts poor survival outcome in gastric cancer patients by SLC7A5 enhancement of tumor growth and metastasis.

Keshuo Ding, Sheng Tan, Xing Huang, Xiaonan Wang, Xiaocan Li, Rong Fan, Yong Zhu, Peter E Lobie, Wenbin Wang, Zhengsheng Wu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

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  6. Mechanisms of resistance to trastuzumab in HER2-positive gastric cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 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

10 authors at 4 institutions in 2 countries.

Keshuo DingFrom the Department of General Surgery, Fourth Affiliated Hospital of Anhui Medical University, 372 Tunxi Road, Hefei, Anhui 230022, China.
Sheng Tanthe Laboratory of Molecular Tumor Pathology, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xing Huangthe Key Laboratory of Precision Diagnosis and Treatment for Hepatobiliary and Pancreatic Tumor of Zhejiang Province, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310006, China.
Xiaonan Wangthe Laboratory of Pathogenic Microbiology and Immunology, Anhui Medical University, Hefei, Anhui 230032, China.
Xiaocan Lithe Department of Pathology and.
Rong Fanthe Laboratory of Molecular Tumor Pathology, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Yong Zhuthe Laboratory of Molecular Tumor Pathology, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Peter E Lobiethe Tsinghua-Berkeley Shenzhen Institute and Division of Life Sciences and Health, Tsinghua University Graduate School, Shenzhen 518055, China, and.
Wenbin WangFrom the Department of General Surgery, Fourth Affiliated Hospital of Anhui Medical University, 372 Tunxi Road, Hefei, Anhui 230022, China, nihao22009256@163.com.
Zhengsheng Wuthe Department of Pathology and woozson@yahoo.com.
Anhui Medical University · CNUniversity of Science and Technology of China · CNNational University of Singapore · SGSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer remains a malignancy with poor survival outcome. We herein report that GSE1, a proline-rich protein, possesses a role in the progression of human gastric cancer. The expression of GSE1 was observed to be much higher in human gastric cancer tissues compared with normal gastric tissues, and GSE1 expression correlated positively with lymph node metastasis, histological grade, depth of invasion, and clinical stage in gastric cancer patients. Moreover, GSE1 expression was also associated with decreased post-operative relapse-free survival and overall survival in the cohort. The forced expression of GSE1 in gastric cancer cell lines resulted in increased cell proliferation, increased colony formation, enhanced cell migration, and invasion. Furthermore, forced expression of GSE1 also increased tumor size and enhanced lung metastasis in xenograft models. The depletion of endogenous GSE1 with shRNAs decreased the oncogenicity and invasiveness of gastric cancer cells both

Indexed as

Cell MovementCell ProliferationAdenocarcinomaAnimalsApoptosisBiomarkers, TumorCase-Control StudiesFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansLarge Neutral Amino Acid-Transporter 1Lymphatic MetastasisMaleMiceMice, Inbred BALB CBiomarkers, TumorGSE1 protein, humanLarge Neutral Amino Acid-Transporter 1Neoplasm Proteinsgastric cancerGSE1metastasismiR-200bmiR-200concogenepathologyproliferationSLC7A5

Identifiers

PMID29367342
PMCPMC5857990
OpenAlexW2784430997

What OpenQuestion holds

Textmetadata
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.