Evidence map›Paper›PMID 39666293›Full record

ArticleJournal of food and drug analysis2022

Diallyl disulfide inhibits proliferation, epithelial-mesenchymal transition, and invasion through RORα-mediated downregulation of Wnt1/β-catenin pathway in gastric cancer cells.

Jian Su, Hui He, Yu-Kun Li, Hong Xia, Fang Liu, Ying Zeng, Xi Zeng, Hui Ling, Bo Su, Qi Su

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of food and drug analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
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

10 authors.

Jian SuDepartment of Pathology, Second Affiliated Hospital, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.
Hui HeHunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.
Yu-Kun LiHunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.
Hong XiaHunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.
Fang LiuHunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.
Ying ZengHunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.
Xi ZengHunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.
Hui LingHunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.
Bo SuHunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.
Qi SuHunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Chang Sheng Xi Avenue 28, Hengyang, Hunan 421001, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overactivation of Wnt/β-catenin pathway due to dysfunction of retinoid-related orphan receptor α (RORα) is related to cancer development and progression. Diallyl disulfide (DADS), an active component of garlic, has been reported in our previous study for upregulation of RORα expression in gastric cancer (GC) cells. It remains to be elucidated the role and mechanism of RORα in DADS against GC. This study revealed that DADS treatment resulted in reduced expression levels of Wnt1, β-catenin, TCF-4, intranuclear β-catenin and p-β-catenin in GC cells, concomitant with the compromised expression of β-catenin target genes (Axin, c-Jun, and c-Myc). RORα overexpression augmented DADS-induced downregulation of Wnt1/β-catenin pathway, G2/M phase arrest, and cell growth inhibition in vitro and in vivo. Contrarily, knockdown of RORα attenuated these effects of DADS. Interestingly, DADS induced an increase in the binding of RORα to β-catenin, which may lead to reduction of β-catenin phosphorylation and nuclear translocation. This interplay modulated by DADS may affect β-catenin target gene expression for that the opposite results were observed in DADS-treated RORα knockdown and overexpression cells. DADS caused a decrease in vimentin, snail and MMP-9, as well as an increase in E-cadherin and TIMP3 expression, which restricted epithelial-mesenchymal transition (EMT), migration, and invasion. The aforementioned effects of DADS were weakened simultaneously when the suppression of DADS on the Wnt1/β-catenin pathway was resisted by knockdown of RORα. In contrast, overexpression of RORα enhanced the effects of DADS. Therefore, RORα-mediated downregulation of Wnt1/β-catenin pathway could undertake an important role in anticancer activity of DADS against GC cell proliferation, EMT, migration, and invasion.

Identifiers

PMID39666293
PMCPMC9635911

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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.