Evidence map›Paper›PMID 35318302›Full record

ArticleNature communications2022

GIT1 protects against breast cancer growth through negative regulation of Notch.

Songbai Zhang, Ayako Miyakawa, Malin Wickström, Cecilia Dyberg, Lauri Louhivuori, Manuel Varas-Godoy, Kati Kemppainen, Shigeaki Kanatani, Dagmara Kaczynska, Ivar Dehnisch Ellström and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  4. [Study on the correlation between high expression of GIT1 and M2 macrophage infiltration and prognosis in hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article
  5. Review
  6. Article
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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

17 authors at 5 institutions in 6 countries.

Songbai ZhangDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-2033-8389
Ayako MiyakawaDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Malin WickströmDepartment of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-5214-9956
Cecilia DybergDepartment of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
Lauri LouhivuoriDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Manuel Varas-GodoyDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-5857-4793
Kati KemppainenTurku Bioscience, Åbo Akademi University and University of Turku, Turku, Finland.
Shigeaki KanataniDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0003-2226-4288
Dagmara KaczynskaDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Ivar Dehnisch EllströmDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Lotta ElfmanDepartment of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
Pauliina KronqvistDepartment of Pathology, University of Turku, Turku, Finland.
Heli RepoDepartment of Pathology, University of Turku, Turku, Finland.
Katsuhiko MikoshibaShanghai Institute for Advanced Immunochemical Studies, ShanghaiTech University, Shanghai, China.ORCID 0000-0002-3487-6970
Cecilia SahlgrenTurku Bioscience, Åbo Akademi University and University of Turku, Turku, Finland.
John Inge JohnsenDepartment of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0003-1277-812X
Per UhlénDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden. per.uhlen@ki.se.ORCID 0000-0003-1446-1062
Karolinska Institutet · SEÅbo Akademi University · FIUniversity of Turku · FIKarolinska University Hospital · SEToho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperactive Notch signalling is frequently observed in breast cancer and correlates with poor prognosis. However, relatively few mutations in the core Notch signalling pathway have been identified in breast cancer, suggesting that as yet unknown mechanisms increase Notch activity. Here we show that increased expression levels of GIT1 correlate with high relapse-free survival in oestrogen receptor-negative (ER(-)) breast cancer patients and that GIT1 mediates negative regulation of Notch. GIT1 knockdown in ER(-) breast tumour cells increased signalling downstream of Notch and activity of aldehyde dehydrogenase, a predictor of poor clinical outcome. GIT1 interacts with the Notch intracellular domain (ICD) and influences signalling by inhibiting the cytoplasm-to-nucleus transport of the Notch ICD. In xenograft experiments, overexpression of GIT1 in ER(-) cells prevented or reduced Notch-driven tumour formation. These results identify GIT1 as a modulator of Notch signalling and a guardian against breast cancer growth.

Indexed as

Breast NeoplasmsAdaptor Proteins, Signal TransducingBreastCell Cycle ProteinsFemaleHumansNeoplasm Recurrence, LocalReceptors, NotchSignal TransductionAdaptor Proteins, Signal TransducingCell Cycle ProteinsGIT1 protein, humanReceptors, Notch

Identifiers

PMID35318302
PMCPMC8940956
OpenAlexW4221027172

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.