Evidence map›Paper›PMID 26770350›Full record

ArticleInternational journal of clinical and experimental medicine2015

Benzyl isothiocyanate inhibits breast cancer cell tumorigenesis via repression of the FoxH1-Mediated Wnt/β-catenin pathway.

Yantao Liu, Lingli Zhang, Yao Meng, Liang Huang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

18 citing papers in PubMed, 25 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

4 authors at 1 institution in 1 country.

Yantao LiuDepartment of Pharmacy, West China Second University Hospital, Sichuan UniversityChengdu 610041, Sichuan, China; Evidence-Based Pharmacy Center, West China Second University Hospital, Sichuan UniversityChengdu 610041, Sichuan, China; Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of EducationChengdu 610041, Sichuan, China.
Lingli ZhangDepartment of Pharmacy, West China Second University Hospital, Sichuan UniversityChengdu 610041, Sichuan, China; Evidence-Based Pharmacy Center, West China Second University Hospital, Sichuan UniversityChengdu 610041, Sichuan, China; Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of EducationChengdu 610041, Sichuan, China.
Yao MengSchool of Medical Laboratory Science, Chengdu Medical College Chengdu 610041, Sichuan, China.
Liang HuangDepartment of Pharmacy, West China Second University Hospital, Sichuan UniversityChengdu 610041, Sichuan, China; Evidence-Based Pharmacy Center, West China Second University Hospital, Sichuan UniversityChengdu 610041, Sichuan, China; Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of EducationChengdu 610041, Sichuan, China.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms underlying the growth inhibitory effect of Benzyl isothiocyanate (BITC) against breast cancer are still not fully understood. Therefore, we further investigated the mechanism in BITC triggering breast cancer. In the present study, we found that the overexpression of FOXH1 in breast cancers tissues and cells, and FOXH1 significantly promoted cell proliferation, invasion and tumorigenesis in vitro. FOXH1 significantly increased the expression levels of β-catenin, cyclinD1, and c-myc proteins in breast cancer cells. Furthermore, siβ-catenin reduced FOXH1 promotion of cell proliferation and invasion in breast cancer cells. Taken together, these results suggest that FOXH1 promoted breast cancer cell growth and invasion by potentiating the Wnt/β-catenin pathway, suggesting that FOXH1 may be a potential molecular target for breast cancer prevention and therapy. Furthermore, BITC treatment has remarkable effect on the expression level of FOXH1 and β-catenin mRNA and protein in MCF-7 cells, MDA-MB-231 cells and SUM 159 cells. BITC treatment has an obvious significance on transcriptional activity of FOXH1. Cell growth and invasion inhibition resulting from BITC exposure were significantly augmented by FoxH1 knockdown. In conclusion, the present study provides novel insights into the molecular circuitry of BITC-induced cell death involving FoxH1-mediated tumorigenesis. Thus, the present study provides a novel insight into the underlying mechanism of tumorigenesis in BITC triggering breast cancer, indicating the therapeutic potential of FOXH1 in the treatment of breast cancer.

Indexed as

Benzyl isothiocyanateFoxH1tumorigenesisWntβ-catenin

Identifiers

PMID26770350
PMCPMC4694250
OpenAlexW2408987926

What OpenQuestion holds

Textmetadata
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.