Evidence map›Paper›PMID 36145166›Full record

ArticleNutrients2022

Wentilactone A Reverses the NF-κB/ECM1 Signaling-Induced Cisplatin Resistance through Inhibition of IKK/IκB in Ovarian Cancer Cells.

Cuiting Lv, Chunxia Ren, Yinjue Yu, Huijing Yin, Caiguo Huang, Gong Yang, Yang Hong

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The Role of Redox Environment in Tumors.Current medicinal chemistry · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. 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

7 authors at 5 institutions in 1 country.

Cuiting LvCentral Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai 200240, China.
Chunxia RenCenter for Reproductive Medicine, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Yinjue YuDepartment of Radiotherapy, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China.
Huijing YinCancer Institute, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Caiguo HuangDepartment of Biochemistry and Molecular Biology, College of Basic Medical, Navy Medical University, Shanghai 200433, China.
Gong YangCentral Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai 200240, China.ORCID 0000-0002-5137-4104
Yang HongCentral Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai 200240, China.
Fudan University · CNFudan University Shanghai Cancer Center · CNShanghai Jiao Tong University · CNShanghai Medical College of Fudan University · CNShanghai University of Traditional Chinese Medicine · CN

Funding

National Natural Science Foundation of China 42076102National Natural Science Foundation of China 81372797National Natural Science Foundation of China 81572553National Natural Science Foundation of China 81772789Natural Science Research Foundation of Minhang District, Shanghai No.2019MHZ041
6 · The paper itself

Abstract

Wentilactone A (WA) is a tetranorditerpenoid isolated from marine algae. We previously found that WA inhibited cancer cell proliferation with little toxicity. In this study, we show that high expression of extracellular matrix protein-1 (ECM1) promotes cancer cell cisplatin resistance, and the secreted ECM1 activates normal fibroblasts (NFs) to transform cells with characteristics of cancer-associated fibroblasts (CAFs). Transcription of the ECM1 gene is regulated largely by NF-κB through EP881C/T-EP266C binding sites. WA supresses the phosphorylation of NF-κB through inhibition of the upstream IKK/IκB phoshorylation to block the expression of ECM1, which reverses the cisplatin-induced activation of NF-κB/ECM1. On the contrary, cisplatin facilitates phosphorylation of NF-κB to enhance the expression of ECM1. These results highlight ECM1 as a potential target for treatment of cisplatin-resistant cancers associated with the ECM1 activated signaling. In addition, WA reverses cisplatin resistance by targeting both tumor cells and the tumor microenvironment through IKK/IκB/NF-κB signaling to reduce the expression of the ECM1 protein.

Indexed as

NF-kappa BOvarian NeoplasmsCarcinoma, Ovarian EpithelialCisplatinExtracellular Matrix ProteinsFemaleHumansI-kappa B KinaseI-kappa B ProteinsPhosphorylationTumor MicroenvironmentCisplatinECM1 protein, humanExtracellular Matrix ProteinsI-kappa B KinaseI-kappa B ProteinsNF-kappa Bcisplatin resistanceNF-κB/ECM1ovarian cancertumor microenvironmentwentilactone A

Identifiers

PMID36145166
PMCPMC9504226
OpenAlexW4296096212

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.