Evidence map›Paper›PMID 24704834›Full record

ArticleOncogene2015

Nuclear SIPA1 activates integrin β1 promoter and promotes invasion of breast cancer cells.

Y Zhang, Y Gong, D Hu, P Zhu, N Wang, Q Zhang, M Wang, A Aldeewan, H Xia, X Qu and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

Y ZhangKey Laboratory of Molecular Biophysics of Ministry of Education, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Y GongDepartment of Breast Surgery, Hubei Cancer Hospital, Wuhan, China.
D HuKey Laboratory of Molecular Biophysics of Ministry of Education, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
P ZhuKey Laboratory of Molecular Biophysics of Ministry of Education, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
N WangKey Laboratory of Molecular Biophysics of Ministry of Education, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Q ZhangKey Laboratory of Molecular Biophysics of Ministry of Education, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
M WangDepartment of Pathology, Hubei Cancer Hospital, Wuhan, China.
A AldeewanKey Laboratory of Molecular Biophysics of Ministry of Education, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
H XiaDepartment of Pathology, Hubei Cancer Hospital, Wuhan, China.
X QuDepartment of Thyroid and Breast Surgery, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
B Z RingInstitute for Genomic and Personalized Medicine, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
N MinatoDepartment of Immunology and Cell Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
L SuKey Laboratory of Molecular Biophysics of Ministry of Education, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Huazhong University of Science and Technology · CNHubei Cancer Hospital · CNKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SIPA1 (signal-induced proliferation-associated protein 1) is a GTPase activation protein that can catalyze the hydrolysis of Rap1 bound GTP to GDP. Recently attention has been paid to a potential role for SIPA1 in cancer metastasis; however, the underlying mechanism of how changes in SIPA1 levels may lead to increased metastasis remains poorly understood. In this study, we showed that SIPA1 was mainly localized to the nuclei in highly invasive breast cancer tumor tissue and MDA-MB-231 cells. Knockdown of SIPA1 in MDA-MB-231 altered cell morphology and cell proliferation ability. Furthermore, this study is the first to establish that nuclear SIPA1 can interact with the integrin β1 promoter and activate its transcription; this interaction appears to be important for SIPA1-dependent MDA-MB-231 cell adhesion and invasion. We also demonstrated that the phosphorylation of FAK, Akt and the expression of MMP9, downstream signaling molecules of integrin β1, were decreased upon SIPA1 knockdown, and MDA-MB-231 cell invasion was impaired. Taken together, these results suggest nuclear SIPA1 contributes to breast cancer cell invasion through the regulation of integrin β1 signaling.

Indexed as

AnimalsAnimals, Genetically ModifiedBreast NeoplasmsCell AdhesionCell Line, TumorCell MovementCell NucleusCell ProliferationFemaleFocal Adhesion Kinase 1GTPase-Activating ProteinsHumansIntegrin beta1Matrix Metalloproteinase 9MCF-7 CellsNeoplasm InvasivenessFocal Adhesion Kinase 1GTPase-Activating ProteinsIntegrin beta1Matrix Metalloproteinase 9MMP9 protein, humanNuclear ProteinsProto-Oncogene Proteins c-aktPTK2 protein, humanRNA, Small InterferingSIPA1 protein, human

Identifiers

PMID24704834
OpenAlexW2003167874

What OpenQuestion holds

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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.