Evidence map›Paper›PMID 31405071›Full record

ArticleNutrients2019

Epigallocatechin-3-Gallate (EGCG) Suppresses Pancreatic Cancer Cell Growth, Invasion, and Migration partly through the Inhibition of Akt Pathway and Epithelial-Mesenchymal Transition: Enhanced Efficacy when Combined with Gemcitabine.

Ran Wei, Natalia E Cortez Penso, Robert M Hackman, Yuefei Wang, Gerardo G Mackenzie

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
6.0field-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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
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  18. Plant-Derived Anti-Cancer Therapeutics and Biopharmaceuticals.Bioengineering (Basel, Switzerland) · 2024
    Review
  19. Review
  20. Drug repurposing for cancer therapy.Signal transduction and targeted therapy · 2024
    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

5 authors at 2 institutions in 2 countries.

Ran WeiTea Science Institute, Zhejiang University, Hangzhou 310058, China.
Natalia E Cortez PensoDepartment of Nutrition, University of California, Davis, CA 95616, USA.
Robert M HackmanDepartment of Nutrition, University of California, Davis, CA 95616, USA.
Yuefei WangTea Science Institute, Zhejiang University, Hangzhou 310058, China. zdcy@zju.edu.cn.com.
Gerardo G MackenzieDepartment of Nutrition, University of California, Davis, CA 95616, USA. ggmackenzie@ucdavis.edu.
University of California, Davis · USTea Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most pancreatic cancers are usually diagnosed at an advanced stage when they have already metastasized. Epigallocatechin-3-gallate (EGCG), a major polyphenolic constituent of green tea, has been shown to reduce pancreatic cancer growth, but its effect on metastasis remains elusive. This study evaluated the capacity of EGCG to inhibit pancreatic cancer cell migration and invasion and the underlying mechanisms. EGCG reduced pancreatic cancer cell growth, migration, and invasion in vitro and in vivo. EGCG prevented "Cadherin switch" and decreased the expression level of TCF8/ZEB1, β-Catenin, and Vimentin. Mechanistically, EGCG inhibited the Akt pathway in a time-dependent manner, by suppressing IGFR phosphorylation and inducing Akt degradation. Co-treatment with catalase or N-Acetyl-L-cysteine did not abrogate EGCG's effect on the Akt pathway or cell growth. Moreover, EGCG synergized with gemcitabine to suppress pancreatic cancer cell growth, migration, and invasion, through modulating epithelial-mesenchymal transition markers and inhibiting Akt pathway. In summary, EGCG may prove beneficial to improve gemcitabine sensitivity in inhibiting pancreatic cancer cell migration and invasion, to some extent through the inhibition of Akt pathway and epithelial-mesenchymal transition.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsCatechinCell Line, TumorCell MovementCell ProliferationDeoxycytidineEnzyme StabilityEpithelial-Mesenchymal TransitionGemcitabineHumansMice, Inbred C57BLNeoplasm InvasivenessPancreatic NeoplasmsProteolysisProto-Oncogene Proteins c-aktCatechinDeoxycytidineepigallocatechin gallateGemcitabineProto-Oncogene Proteins c-aktAktEMTepigallocatechin-3-gallategemcitabinepancreatic cancer

Identifiers

PMID31405071
PMCPMC6722696
OpenAlexW2968952801

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.