Evidence map›Paper›PMID 29202800›Full record

ArticleBMC cancer2017

Genistein induces apoptosis of colon cancer cells by reversal of epithelial-to-mesenchymal via a Notch1/NF-κB/slug/E-cadherin pathway.

Panpan Zhou, Chunling Wang, Zebin Hu, Wenruo Chen, Wentao Qi, Aike Li

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
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  7. Cellular and Molecular Mechanisms Modulated by Genistein in Cancer.International journal of molecular sciences · 2025
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  18. Journal of gastrointestinal oncology · 2023
    Article
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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

6 authors at 3 institutions in 1 country.

Panpan ZhouCereals & Oils Nutrition Research Group, Academy of State Administration of Grain (ASAG), No.11 Baiwanzhuang Street, Beijing, 100037, People's Republic of China.
Chunling WangKey Laboratory of Food Safety and Sanitation, Ministry of Education, College of Food Engineering and Biotechnology, Tianjin University of Science and Technology, Tianjin, People's Republic of China.
Zebin HuInstitue for In Vitro Diagnostic Reagents Control, the National Institutes for food and drug Control (NIFDC), Beijing, 100050, People's Republic of China.
Wenruo ChenCereals & Oils Nutrition Research Group, Academy of State Administration of Grain (ASAG), No.11 Baiwanzhuang Street, Beijing, 100037, People's Republic of China.
Wentao QiCereals & Oils Nutrition Research Group, Academy of State Administration of Grain (ASAG), No.11 Baiwanzhuang Street, Beijing, 100037, People's Republic of China. qwt@chinagrain.org.
Aike LiCereals & Oils Nutrition Research Group, Academy of State Administration of Grain (ASAG), No.11 Baiwanzhuang Street, Beijing, 100037, People's Republic of China.
Academy of State Administration of Grain · CNNational Institutes for Food and Drug Control · CNTianjin University of Science and Technology · CN

Funding

National Natural Science Foundation of China No. 31471591
6 · The paper itself

Abstract

backgroundGenistein has been known to inhibit proliferation and induce apoptosis in several kinds of cancer cells. While knowledge of genistein in regulating epithelial mesenchymal transition (EMT) of colon cancer cells is unknown.

methodsTo investigate the effects and mechanisms of genistein on EMT of colon cancer cells, HT-29 cells were used and treated by genistein and TNF-α in this paper. EMT was determined by cell invasion assays using a transwell chamber and the expression changes of EMT-related markers were confirmed by RT-PCR, Western blotting, and immunofluorescence staining.

resultsGenistein inhibited cell migration at 200 μmol/L. Genistein reversed the EMT of colon cancer cells by upregulation of E-cadherin and downregulation of N-cadherin, accompanied by the suppression of EMT related makers, such as Snail2/slug, ZEB1, ZEB2, FOXC1, FOXC2 and TWIST1. Moreover, genistein can inhibit the expression of notch-1, p-NF-κB and NF-κB, while promote the expression of Bax/Bcl-2 and caspase-3 in HT-29 cells.

conclusionThe present study demonstrated that genistein suppressed the migration of colon cancer cells by reversal the EMT via suppressing the Notch1/NF-κB/slug/E-cadherin pathway. Genistein may be developed as a potential antimetastasis agent to colon cancer.

Indexed as

Antigens, CDAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsCadherinsCell MovementCell ProliferationColonic NeoplasmsDrug Screening Assays, AntitumorEpithelial-Mesenchymal TransitionGene ExpressionGenisteinHT29 CellsHumansNF-kappa BReceptor, Notch1Antigens, CDAntineoplastic AgentsApoptosis Regulatory ProteinsCadherinsCDH1 protein, humanGenisteinNF-kappa BNOTCH1 protein, humanReceptor, Notch1RELA protein, humanSNAI1 protein, humanSnail Family Transcription FactorsTranscription Factor RelAApoptosisColon cancer cellEpithelial mesenchymal transitionGenistein

Identifiers

PMID29202800
PMCPMC5715491
OpenAlexW2771654374

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.