Evidence map›Paper›PMID 30858760›Full record

ArticleCancer cell international2019

Epigallocatechin-3-gallate inhibits the growth and increases the apoptosis of human thyroid carcinoma cells through suppression of EGFR/RAS/RAF/MEK/ERK signaling pathway.

Dongdong Wu, Zhengguo Liu, Jianmei Li, Qianqian Zhang, Peiyu Zhong, Tieshan Teng, Mingliang Chen, Zhongwen Xie, Ailing Ji, Yanzhang Li

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  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

10 authors at 2 institutions in 1 country.

Dongdong Wu1School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, 475004 Henan China.ORCID 0000-0001-6739-8437
Zhengguo Liu1School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, 475004 Henan China.
Jianmei Li1School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, 475004 Henan China.
Qianqian Zhang1School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, 475004 Henan China.
Peiyu Zhong1School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, 475004 Henan China.
Tieshan Teng1School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, 475004 Henan China.
Mingliang Chen1School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, 475004 Henan China.
Zhongwen Xie2State Key Laboratory of Tea Plant Biology and Utilization, Anhui Agricultural University, 130 Changjiang West Road, Hefei, 230036 Anhui China.
Ailing Ji1School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, 475004 Henan China.
Yanzhang Li1School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, 475004 Henan China.
Henan University · CNAnhui Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThyroid cancer is the most common type of endocrine malignancy and the incidence rate is rapidly increasing worldwide. Epigallocatechin-3-gallate (EGCG) could suppress cancer growth and induce apoptosis in many types of cancer cells. However, the mechanism of action of EGCG on the growth of human thyroid carcinoma cells has not been fully illuminated.

methodsCell proliferation and viability were detected by EdU and MTS assays. Cell cycle distribution was measured by flow cytometry. Migration and invasion were evaluated by scratch and transwell assays. Apoptotic levels were detected by TUNEL staining and western blotting. The protein levels of EGFR/RAS/RAF/MEK/ERK signaling pathway were detected by western blotting. The in vivo results were determined by tumor xenografts in nude mice. The in vivo proliferation, tumor microvessel density, and apoptosis were detected by immunohistochemistry.

resultsEGCG inhibited the proliferation, viability, and cell cycle progression in human thyroid carcinoma cells. EGCG decreased the migration and invasion, but increased the apoptosis of human thyroid carcinoma cells. EGCG reduced the protein levels of phospho (p)-epidermal growth factor receptor (EGFR), H-RAS, p-RAF, p-MEK1/2, and p-extracellular signal-regulated protein kinase 1/2 (ERK1/2) in human thyroid carcinoma cells. EGCG inhibited the growth of human thyroid carcinoma xenografts by inducing apoptosis and down-regulating angiogenesis.

conclusionsEGCG could reduce the growth and increase the apoptosis of human thyroid carcinoma cells through suppressing the EGFR/RAS/RAF/MEK/ERK signaling pathway. EGCG can be developed as an effective therapeutic agent for the treatment of thyroid cancer.

Indexed as

AngiogenesisApoptosisEGCGSignaling pathwayThyroid carcinoma

Identifiers

PMID30858760
PMCPMC6394055
OpenAlexW2918424518

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.