Evidence map›Paper›PMID 27345400›Full record

ArticleOncogene2017

KRT19 directly interacts with β-catenin/RAC1 complex to regulate NUMB-dependent NOTCH signaling pathway and breast cancer properties.

S K Saha, H Y Choi, B W Kim, A A Dayem, G-M Yang, K S Kim, Y F Yin, S-G Cho

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

94 citing papers in PubMed, 138 citations in OpenAlex.

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34 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

S K SahaDepartment of Animal Biotechnology, Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, Seoul, Republic of Korea.
H Y ChoiDepartment of Animal Biotechnology, Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, Seoul, Republic of Korea.
B W KimDepartment of Animal Biotechnology, Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, Seoul, Republic of Korea.
A A DayemDepartment of Animal Biotechnology, Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, Seoul, Republic of Korea.
G-M YangDepartment of Animal Biotechnology, Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, Seoul, Republic of Korea.
K S KimDepartment of Animal Biotechnology, Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, Seoul, Republic of Korea.
Y F YinDepartment of Animal Biotechnology, Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, Seoul, Republic of Korea.
S-G ChoDepartment of Animal Biotechnology, Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, Seoul, Republic of Korea.
Konkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies have reported that interactions between keratins (KRTs) and other proteins initiate signaling cascades that regulate cell migration, invasion, and metastasis. In the current study, we found that expression of KRT19 was specifically high in breast cancers and significantly correlated with their invasiveness. Moreover, knockdown of KRT19 led to increased proliferation, migration, invasion, drug resistance, and sphere formation in breast cancer cells via an upregulated NOTCH signaling pathway. This was owing to reduced expression of NUMB, an inhibitory protein of the NOTCH signaling pathway. In addition, we found that KRT19 interacts with β-catenin/RAC1 complex and enhances the nuclear translocation of β-catenin. Concordantly, knockdown of KRT19 suppressed the nuclear translocation of β-catenin as well as β-catenin-mediated NUMB expression. Furthermore, modulation of KRT19-mediated regulation of NUMB and NOTCH1 expression led to the repression of the cancer stem cell properties of breast cancer patient-derived CD133

Indexed as

Animalsbeta CateninBreast NeoplasmsCell Line, TumorCell MovementCell NucleusCell ProliferationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHep G2 CellsHumansKeratin-19MCF-7 CellsMembrane ProteinsMicebeta CateninCTNNB1 protein, humanKeratin-19Membrane ProteinsNerve Tissue ProteinsNUMB protein, humanrac1 GTP-Binding ProteinRAC1 protein, humanReceptors, Notch

Identifiers

PMID27345400
PMCPMC5270332
OpenAlexW2472173303

What OpenQuestion holds

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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.