Evidence map›Paper›PMID 26468779›Full record

ArticleScientific reports2015

Elevation of ω-3 Polyunsaturated Fatty Acids Attenuates PTEN-deficiency Induced Endometrial Cancer Development through Regulation of COX-2 and PGE2 Production.

Jinshun Pan, Lixian Cheng, Xinyun Bi, Xin Zhang, Shanshan Liu, Xiaoming Bai, Fanghong Li, Allan Z Zhao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. UterineCancers · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Modeling Endometrial Cancer: Past, Present, and Future.International journal of molecular sciences · 2018
    Review
  12. Article
  13. Article
  14. 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

8 authors at 1 institution in 1 country.

Jinshun PanThe Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.
Lixian ChengThe Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.
Xinyun BiThe Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.
Xin ZhangThe Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.
Shanshan LiuThe Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.
Xiaoming BaiCancer Center, Department of Pathology, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.
Fanghong LiThe Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.
Allan Z ZhaoThe Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometrial cancer is one of the most common gynecologic malignancies. Phosphatase and tensin homologue (PTEN)-mutation is frequently identified in endometrial cancer patients. Although high dietary intake of ω-3 polyunsaturated fatty acids (PUFAs) has been associated with reduced risk of endometrial cancer, the underlying mechanisms is still unknown. To this end, we evaluated the impact of ω-3 PUFAs using several endometrial cancer cellular and animal models. While ~27% and 40% of heterozygotic PTEN mutant mice developed endometrial cancer and atypical complex hyperplasia, respectively, none of the PTEN(+/-) mice developed cancer when we overexpressed an mfat-1 transgene, which allowed endogenous production of ω-3 PUFAs. Fish oil-enriched diet or expression of mfat-1 transgene significantly inhibited the growth of xenograft tumor derived from RL95-2 cells bearing a PTEN null mutation. At cellular level, ω-3 PUFAs treatment decreased the viability of RL95-2 cells, AKT phosphorylation, and cyclin D1 expression. These molecular events are primarily mediated through reduction of cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) production. Exogenous PGE2 treatment completely blunted the impact of ω-3 PUFAs on endometrial cancer. Thus, we revealed the direct inhibitory effects of ω-3 PUFAs on endometrial cancer development and the underlying mechanisms involving reduction of COX-2 and PGE2.

Indexed as

AnimalsCadherinsCell CycleCell Line, TumorCell ProliferationCell Transformation, NeoplasticCyclin D1Cyclooxygenase 2DinoprostoneDisease Models, AnimalEicosanoidsEndometrial NeoplasmsFatty Acids, Omega-3FemaleGene ExpressionHeterograftsCadherinsCyclin D1Cyclooxygenase 2DinoprostoneEicosanoidsfat1 protein, mouseFatty Acids, Omega-3Proto-Oncogene Proteins c-aktPTEN Phosphohydrolase

Identifiers

PMID26468779
PMCPMC4606560
OpenAlexW2412256764

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.