Evidence map›Paper›PMID 31933724›Full record

ArticleInternational journal of clinical and experimental pathology2019

NF-κB/Twist axis is involved in chysin inhibition of ovarian cancer stem cell features induced by co-treatment of TNF-α and TGF-β.

Huazhen Li, A Chen, Qiaoqi Yuan, Weifeng Chen, Huimin Zhong, Mo Teng, Chang Xu, Yebei Qiu, Jianguo Cao

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
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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

9 authors at 2 institutions in 1 country.

Huazhen LiDepartment of Gynecology and Obstetrics, The Second Affiliated Hospital of Guangzhou Medical University 511447, Guangdong, China.
A ChenDepartment of Pharmaceutical Science, Medical College, Hunan Normal University, Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province Changsha 410013, China.
Qiaoqi YuanDepartment of Gynecology and Obstetrics, The Second Affiliated Hospital of Guangzhou Medical University 511447, Guangdong, China.
Weifeng ChenDepartment of Gynecology and Obstetrics, The Second Affiliated Hospital of Guangzhou Medical University 511447, Guangdong, China.
Huimin ZhongDepartment of Gynecology and Obstetrics, The Second Affiliated Hospital of Guangzhou Medical University 511447, Guangdong, China.
Mo TengDepartment of Gynecology and Obstetrics, The Second Affiliated Hospital of Guangzhou Medical University 511447, Guangdong, China.
Chang XuDepartment of Pharmaceutical Science, Medical College, Hunan Normal University, Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province Changsha 410013, China.
Yebei QiuDepartment of Pharmaceutical Science, Medical College, Hunan Normal University, Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province Changsha 410013, China.
Jianguo CaoDepartment of Pharmaceutical Science, Medical College, Hunan Normal University, Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province Changsha 410013, China.
Second Affiliated Hospital of Guangzhou Medical University · CNHunan Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chrysin (ChR) inhibits various cancer cells and possesses anti-inflammatory activities. NF-kB has been shown to regulate the expression of genes involved in epithelial-mesenchymal transformation (EMT) by upregulation of TWIST1. This study aimed to assess whether ChR can inhibit EMT phenotype and cancer stem-like cell (CSLC) features in ovarian cancer cells co-treated with TNF-α and TGF-β. Here, OVCAR-3 cells were co-treated with TNF-α and TGF-β in the presence or absence of ChR. Then, the expression levels of E-cadherin, N-cadherin, CD133, CD44, NF-κBp65, and TWIST1 were analyzed by western blotting. Wound healing and tumor sphere formation assays were performed to assess the migration and sphere-forming capabilities of cells, respectively. Overexpression and/or knockdown of NF-κBp65 and/or TWIST1 were used to explore the molecular mechanisms. We showed that ChR inhibited EMT and CSLC properties in ovarian cancer cells administered TNF-α after prolonged TGF-β treatment, in a dose-dependent manner. Also, knockdown of NF-κBp65 and ChR cooperatively enhanced the inhibition of NF-κBp65 and TWIST1 expression, EMT phenotype, and CSLC properties. Conversely, overexpression of NF-κBp65 antagonized the above-mentioned activities of ChR. Furthermore, TWIST1 silencing or overexpression did not affect the ChR treatment effect on NF-κBp65 levels, but it reduced or enhanced EMT and CSLC properties. In conclusion, ChR can inhibit a proinflammatory cytokine to induce EMT and CSLC characteristics in OVCAR-3 cells, which may be involved in blocking the NF-κB/Twist axis.

Indexed as

cancer stem cellschrysinepithelial-mesenchymal transitionNF-κBOvarian cancerTWIST1

Identifiers

PMID31933724
PMCPMC6943996
OpenAlexW3024306113

What OpenQuestion holds

Textmetadata
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.