Evidence map›Paper›PMID 32236585›Full record

ArticleOncology reports2020

PTEN/AKT/mTOR signaling mediates anticancer effects of epigallocatechin‑3‑gallate in ovarian cancer.

Jianli Qin, Minglei Fu, Juan Wang, Fengxiang Huang, Haiping Liu, Mengjie Huangfu, Dan Yu, Haowei Liu, Xumei Li, Xiao Guan and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Epicatechin DecreasesInternational journal of molecular sciences · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. The Interplay between Autophagy and Mitochondria in Cancer.International journal of molecular sciences · 2024
    Review
  20. 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

11 authors at 1 institution in 1 country.

Jianli Qin *College of Pharmacy, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Minglei Fu *Dispensary, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Juan WangResearch Center for Science, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Fengxiang HuangCollege of Pharmacy, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Haiping LiuScience and Technology Department, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Mengjie HuangfuCollege of Pharmacy, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Dan YuCollege of Pharmacy, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Haowei LiuCollege of Pharmacy, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Xumei LiCollege of Pharmacy, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Xiao GuanCollege of Pharmacy, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Xu ChenCollege of Pharmacy, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
Guilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigallocatechin‑3‑gallate (EGCG), a polyphenol present in green tea, exhibits anticancer effects in various types of cancer. A number of studies have focused on the effects of EGCG on lung cancer, but not ovarian cancer. Previous reports have implicated that EGCG suppressed ovarian cancer cell proliferation and induced apoptosis, but its potential anticancer mechanisms and signaling pathways remain unclear. Thus, it is necessary to determine the anti‑ovarian cancer effects of EGCG and explore the underlying mechanisms. In the present study, EGCG exerted stronger proliferation inhibition on SKOV3 cells compared with A549 cells and induced apoptosis in SKOV3 cells, as well as upregulated PTEN expression and downregulated the expression of phosphoinositide‑dependent kinase‑1 (PDK1), phosphor (p)‑AKT and p‑mTOR. These effects were reversed by the PTEN inhibitor VO‑Ohpic trihydrate. The results of the mouse xenograft experiment demonstrated that 50 mg/kg EGCG exhibited increased tumor growth inhibition compared with 5 mg/kg paclitaxel. In addition, PTEN expression was upregulated, whereas the expression levels of PDK1, p‑AKT and p‑mTOR were downregulated in the EGCG treatment group compared with those in untreated mice in vivo. In conclusion, the results of the present study provided a new underlying mechanism of the effect of EGCG on ovarian cancer and may lead to the development of EGCG as a candidate drug for ovarian cancer therapy.

Indexed as

A549 CellsAnimalsAntineoplastic Agents, PhytogenicCatechinCell Line, TumorCell ProliferationCell SurvivalFemaleGene Expression Regulation, NeoplasticHumansMiceOvarian NeoplasmsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionTOR Serine-Threonine KinasesAntineoplastic Agents, PhytogenicCatechinepigallocatechin gallateMTOR protein, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine Kinasesapoptosisepigallocatechin-3-gallateovarian cancerproliferationVO-Ohpic trihydrate

Identifiers

PMID32236585
PMCPMC7160558
OpenAlexW3014793247

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.