Evidence map›Paper›PMID 26320193›Full record

ArticleOncotarget2015

S100P interacts with integrin α7 and increases cancer cell migration and invasion in lung cancer.

Ya-Ling Hsu, Jen-Yu Hung, Yung-Yu Liang, Yi-Shiuan Lin, Ming-Ju Tsai, Shah-Hwa Chou, Chi-Yu Lu, Po-Lin Kuo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  10. Molecular and Clinicopathologic Impact of GNAS Variants Across Solid Tumors.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024
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  14. Inhibition of the ITGB1 gene attenuates crystalline silica-induced pulmonary fibrosis via epithelial-mesenchymal transformation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 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

8 authors at 3 institutions in 1 country.

Ya-Ling HsuGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Jen-Yu HungDivision of Pulmonary and Critical Care Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Yung-Yu LiangGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Yi-Shiuan LinGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Ming-Ju TsaiGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Shah-Hwa ChouDivision of Chest Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Chi-Yu LuDepartment of Biochemistry, Kaohsiung Medical University, Kaohsiung, Taiwan.
Po-Lin KuoInstitute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Kaohsiung Medical University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWNational Sun Yat-sen University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

S100P, a Ca2+ binding protein, has been shown to be overexpressed in various cancers. However, its functional character in lung cancer remains largely unknown. In this study, we show that S100P increases cancer migration, invasion and metastasis in lung cancer cells. Ectopic expression of S100P increases migration, invasion and EMT in less invasive CL1-0 lung cancer cells. Conversely, knockdown of S100P suppressed migration and invasion, and caused a reversion of EMT in highly invasive lung cancer cells. These effects were transduced by increasing the interaction of S100P with integrin α7, which activated focal adhesion kinase (FAK) and AKT. Blocking FAK significantly decreased S100P-induced migration by decreasing Src and AKT activation, whereas inhibiting AKT reduced S100P upregulation on ZEB1 expression. Further study has indicated that S100P knockdown prevents the spread of highly metastatic human lung cancer in animal models. This study therefore suggests that S100P represents a critical activator of lung cancer metastasis. Detection and targeted treatment of S100P-expressing cancer is an attractive therapeutic strategy in treating lung cancer.

Indexed as

Cell MovementAnimalsAntigens, CDCalcium-Binding ProteinsCell Line, TumorFemaleFocal Adhesion Protein-Tyrosine KinasesGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansImmunoblottingIntegrin alpha ChainsLung NeoplasmsMaleMice, NudeMicroscopy, ConfocalAntigens, CDCalcium-Binding ProteinsFocal Adhesion Protein-Tyrosine KinasesHomeodomain Proteinsintegrin alpha7Integrin alpha ChainsNeoplasm ProteinsProto-Oncogene Proteins c-aktS100P protein, humanTranscription FactorsZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1FAKmetastasisoncogeneS100PZEB1

Identifiers

PMID26320193
PMCPMC4745748
OpenAlexW1224395538

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.