Evidence map›Paper›PMID 37787987›Full record

ArticleAging2023

Eriocitrin inhibits epithelial-mesenchymal transformation (EMT) in lung adenocarcinoma cells via triggering ferroptosis.

Minglang Gao, Kai Lai, Yu Deng, Zilong Lu, Congkuan Song, Wenjie Wang, Chenzhen Xu, Ning Li, Qing Geng

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
8.3field-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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Journal of oral microbiology · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. 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

9 authors at 3 institutions in 1 country.

Minglang GaoDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Kai LaiDepartment of Cardiothoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330000, China.
Yu DengDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Zilong LuDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Congkuan SongDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Wenjie WangDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Chenzhen XuDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Ning LiDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Qing GengDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Wuhan University · CNRenmin Hospital of Wuhan University · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionLung adenocarcinoma (LUAD) is the most prevalent pathological subtype of non-small cell lung cancer (NSCLC), characterized by a high propensity for relapse and metastasis due to epithelial-mesenchymal transition (EMT) of cancer cells. Ferroptosis, a newly discovered regulated cell death modality, is interconnected with the EMT process in certain cancers. Eriocitrin, a natural flavonoid compound, exerts anti-inflammatory and anticancer effects.

objectivesThe aim of this study is to investigate the potential inhibitory effect of eriocitrin on lung adenocarcinoma metastasis and explore whether its underlying mechanism involves ferroptosis induction in cancer cells.

methodsThe CCK8 assay and wound healing assay and transwell were conducted to determine the cell viability and migration ability of A549 and H1299 cells, respectively. EMT process was assessed by western blot and RT-PCR to detect protein and mRNA levels of EMT markers. ROS and cell iron were measured to determine ferroptosis level.

resultsEriocitrin treatment significantly inhibited cell viability and migration ability in a concentration-dependent manner. Furthermore, eriocitrin administration for 24 hours resulted in enhanced expression of E-cadherin, while downregulating vimentin, N-cadherin and snail expression, indicating marked repression of the EMT process. Additionally, eriocitrin significantly induced ferroptosis in A549 and H1299 cells, as evidenced by increased ROS levels, downregulation of Nrf-2, SLC7A11 and GPX4 expression, and enhanced cellular iron accumulation. Moreover, pretreatment with the ferroptosis inhibitor ferrostatin-1 effectively abrogated the inhibitory effects of eriocitrin on EMT.

conclusionsOur findings further support the anti-cancer properties of eriocitrin, as evidenced by its ability to inhibit the EMT process in LUAD cells, which is partially mediated through induction of ferroptosis in cancer cells.

Indexed as

Adenocarcinoma of LungCarcinoma, Non-Small-Cell LungFerroptosisLung NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFlavanonesHumansIronNeoplasm Recurrence, LocalReactive Oxygen SpecieseriocitrinFlavanonesIronReactive Oxygen SpecieschemopreventiveEMTeriocitrinferroptosisLUADmetastasis

Identifiers

PMID37787987
PMCPMC10599723
OpenAlexW4387267865

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.