Evidence map›Paper›PMID 26202299›Full record

ArticleScientific reports2015

Blockade of Wnt/β-catenin signaling suppresses breast cancer metastasis by inhibiting CSC-like phenotype.

Gyu-Beom Jang, Ji-Young Kim, Sung-Dae Cho, Ki-Soo Park, Ji-Youn Jung, Hwa-Yong Lee, In-Sun Hong, Jeong-Seok Nam

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing papers in PubMed, 1 pooled it
15.1field-weighted citation impact, top 1% 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

213 citing papers in PubMed, 1 synthesis or guideline pooled it, 320 citations in OpenAlex.

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153 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 5 institutions in 1 country.

Gyu-Beom Jang1] Laboratory of Tumor Suppressor, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, 406-840, Republic of Korea [2] Department of Molecular Medicine, School of Medicine, Gachon University, Incheon 406-840, Republic of Korea.
Ji-Young Kim1] Laboratory of Tumor Suppressor, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, 406-840, Republic of Korea [2] Department of Molecular Medicine, School of Medicine, Gachon University, Incheon 406-840, Republic of Korea.
Sung-Dae ChoDepartment of Oral Pathology, School of Dentistry, and Institute of Oral Bioscience, Chonbuk National University, Jeonju, Republic of Korea.
Ki-Soo ParkDepartment of New Technology Development, Korea Health Industry Development Institute (KHIDI), Cheongju-si 363-700, Republic of Korea.
Ji-Youn JungDepartment of Companion and Laboratory Animal Science, Kongju National University, Chungnam 314-702, Republic of Korea.
Hwa-Yong LeeThe Faculty of Liberal Arts, Jungwon University, Chungbuk, 367-805, Republic of Korea.
In-Sun Hong1] Laboratory of Tumor Suppressor, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, 406-840, Republic of Korea [2] Department of Molecular Medicine, School of Medicine, Gachon University, Incheon 406-840, Republic of Korea.
Jeong-Seok Nam1] Laboratory of Tumor Suppressor, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, 406-840, Republic of Korea [2] Department of Molecular Medicine, School of Medicine, Gachon University, Incheon 406-840, Republic of Korea.
Gachon University · KRJeonbuk National University · KRJungwon University · KRKongju National University · KRKorea Health Industry Development Institute · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The identification of cancer stem cells (CSCs) represents an important milestone in the understanding of chemodrug resistance and cancer recurrence. More specifically, some studies have suggested that potential metastasis-initiating cells (MICs) might be present within small CSC populations. The targeting and eradication of these cells represents a potential strategy for significantly improving clinical outcomes. A number of studies have suggested that dysregulation of Wnt/β-catenin signaling occurs in human breast cancer. Consistent with these findings, our previous data have shown that the relative level of Wnt/β-catenin signaling activity in breast cancer stem cells (BCSCs) is significantly higher than that in bulk cancer cells. These results suggest that BCSCs could be sensitive to therapeutic approaches targeting Wnt/β-catenin signaling pathway. In this context, abnormal Wnt/β-catenin signaling activity may be an important clinical feature of breast cancer and a predictor of poor survival. We therefore hypothesized that Wnt/β-catenin signaling might regulate self-renewal and CSC migration, thereby enabling metastasis and systemic tumor dissemination in breast cancer. Here, we investigated the effects of inhibiting Wnt/β-catenin signaling on cancer cell migratory potential by examining the expression of CSC-related genes, and we examined how this pathway links metastatic potential with tumor formation in vitro and in vivo.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorDose-Response Relationship, DrugFemaleFrizzled-Related ProteinsGlycoproteinsIntracellular Signaling Peptides and ProteinsMiceMice, Inbred BALB CNeoplastic Stem CellsSulfonamidesTreatment OutcomeWnt Signaling PathwayFH535Frizzled-Related ProteinsGlycoproteinsIntracellular Signaling Peptides and ProteinsSulfonamides

Identifiers

PMID26202299
PMCPMC5378883
OpenAlexW2407520682

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.