Evidence map›Paper›PMID 30584245›Full record

ArticleCell death & disease2018

Estrogen affects the negative feedback loop of PTENP1-miR200c to inhibit PTEN expression in the development of endometrioid endometrial carcinoma.

Ruichao Chen, Minfen Zhang, Wenya Liu, Hui Chen, Tonghui Cai, Hanzhen Xiong, Xiujie Sheng, Shaoyan Liu, Juan Peng, Fang Wang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. PRMT7-Mediated PTEN Activation Enhances Bone Regeneration in Female Mice.International journal of molecular sciences · 2025
    Article
  7. Article
  8. Advances in MiRNAs Involved in Endometrial Carcinoma.Combinatorial chemistry & high throughput screening · 2025
    Review
  9. Article
  10. Review
  11. Cancers · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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

15 authors at 3 institutions in 2 countries.

Ruichao ChenDepartment of Pathology, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Minfen ZhangDepartment of Pathology, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Wenya LiuDepartment of Pathology, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Hui ChenDepartment of Pathology, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Tonghui CaiDepartment of Pathology, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Hanzhen XiongDepartment of Pathology, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Xiujie ShengKey Laboratory of Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Shaoyan LiuDepartment of Pathology, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Juan PengDepartment of Pathology, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Fang WangKey Laboratory of Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China.
Hao ChenDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX75390, USA.
Wanrun LinDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX75390, USA.
Xuehu XuKey Laboratory of Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China. maxtiger@126.com.
Wenxin ZhengDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX75390, USA. wenxin.zheng@utsouthwestern.edu.
Qingping JiangDepartment of Pathology, The Third Affiliated Hospital, Guangzhou Medical University, 510150, Guangzhou, China. jiangqingping@gzhmu.edu.cn.
Guangzhou Medical University · CNThird Affiliated Hospital of Guangzhou Medical University · CNThe University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometrial carcinoma is one of the most common malignancies in the female reproductive system. It is well-known that estrogen plays an important role in the pathogenesis of endometrioid endometrial carcinoma (EEC), and induces the cancer suppressor gene PTEN deletion. However, how estrogen affects PTEN expression remains unknown. In the present study, we found in 40 EEC specimens, miR-200c level was higher in most cancer areas than that in the adjacent normal endometrium, while PTEN and PTENP1 were lower. Moreover, the expression of PTEN/PTENP1 and miR-200c also showed a converse relationship in EEC cell lines. In addition, we demonstrated that miR-200c bound directly to PTEN and PTENP1, and PTENP1 could reverse miR-200c inhibition function to PTEN using a dual-luciferase reporter and RNA binding protein immunoprecipitation (RIP) assays. Next, 17β-estradiol (E2) treatment could improve miR-200c and drop the PTEN level, which caused a consequential increase of the phospho-PI3K-AKT pathway genes. When we stably knocked down estrogen receptor α (ERα) expression in the EEC cell line, the effects of E2 on miR-200c and PTEN declined. In addition, it was demonstrated that E2 might modulate cell proliferation, migration and invasion relying on the expression of miR-200c. Taken together, it can be concluded that estrogen improves the miR-200c level by combining with ER, PTENP1 and PTEN could be inhibited by miR-200c, and then activate the PI3K-AKT pathway. This work provided a new mechanism of EEC development and a new potential therapeutic target.

Indexed as

Carcinoma, EndometrioidCell Line, TumorEndometrial NeoplasmsEstrogensFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRNA, NeoplasmSignal TransductionEstrogensMicroRNAsMIRN200 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanRNA, Neoplasm

Identifiers

PMID30584245
PMCPMC6315040
OpenAlexW2904444783

What OpenQuestion holds

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Registered trials

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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.