Evidence map›Paper›PMID 26750754›Full record

ArticleScientific reports2016

A novel cell-penetrating peptide suppresses breast tumorigenesis by inhibiting β-catenin/LEF-1 signaling.

Tsung-Hua Hsieh, Chia-Yi Hsu, Cheng-Fang Tsai, Chien-Chih Chiu, Shih-Shin Liang, Tsu-Nai Wang, Po-Lin Kuo, Cheng-Yu Long, Eing-Mei Tsai

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

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  14. A Synthetic CPP33-ConjugatedBiomolecules · 2020
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  15. The Role of Interleukin-9 in Cancer.Pathology oncology research : POR · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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

9 authors at 1 institution in 1 country.

Tsung-Hua HsiehDepartment of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Chia-Yi HsuGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Cheng-Fang TsaiGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Chien-Chih ChiuResearch Center for Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Shih-Shin LiangResearch Center for Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Tsu-Nai WangResearch Center for Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Po-Lin KuoResearch Center for Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Cheng-Yu LongDepartment of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Eing-Mei TsaiDepartment of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Kaohsiung Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inhibition of β-catenin/LEF-1 signaling is an emerging strategy in cancer therapy. However, clinical targeted treatment of the β-catenin/LEF-1 complex remains relatively ineffective. Therefore, development of specific molecular targets is a key approach for identifying new cancer therapeutics. Thus, we attempted to synthesize a peptide (TAT-NLS-BLBD-6) that could interfere with the interaction of β-catenin and LEF-1 at nuclei in human breast cancer cells. TAT-NLS-BLBD-6 directly interacted with β-catenin and inhibited breast cancer cell growth, invasion, migration, and colony formation as well as increased arrest of sub-G1 phase and apoptosis; it also suppressed breast tumor growth in nude mouse and zebrafish xenotransplantation models, showed no signs of toxicity, and did not affect body weight. Furthermore, the human global gene expression profiles and Ingenuity Pathway Analysis software showed that the TAT-NLS-BLBD-6 downstream target genes were associated with the HER-2 and IL-9 signaling pathways. TAT-NLS-BLBD-6 commonly down-regulated 27 candidate genes in MCF-7 and MDA-MB-231 cells, which are concurrent with Wnt downstream target genes in human breast cancer. Our study suggests that TAT-NLS-BLBD-6 is a promising drug candidate for the development of effective therapeutics specific for Wnt/β-catenin signaling inhibition.

Indexed as

Signal TransductionAnimalsApoptosisbeta CateninBreast NeoplasmsCell Line, TumorCell MovementCell NucleusCell-Penetrating PeptidesCell ProliferationCell Transformation, NeoplasticDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticHumansLymphoid Enhancer-Binding Factor 1beta CateninCell-Penetrating PeptidesLymphoid Enhancer-Binding Factor 1Nuclear Localization SignalsRecombinant Fusion Proteinstat Gene Products, Human Immunodeficiency Virus

Identifiers

PMID26750754
PMCPMC4707489
OpenAlexW2419350902

What OpenQuestion holds

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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.