Evidence map›Paper›PMID 27862996›Full record

ArticleJournal of cellular and molecular medicine2017

Tannic acid inhibits EGFR/STAT1/3 and enhances p38/STAT1 signalling axis in breast cancer cells.

Pramod Darvin, Youn Hee Joung, Dong Young Kang, Nipin Sp, Hyo Joo Byun, Tae Sook Hwang, Hema Sasidharakurup, Chi Ho Lee, Kwang Hyun Cho, Kyung Do Park and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  6. Screening andAnti-cancer agents in medicinal chemistry · 2025
    Article
  7. Article
  8. Antifungal activity of tannic acid against Candida spp. and its mechanism of action.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2024
    Article
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  12. Review
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  17. Review
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  20. JAK-STAT core cancer pathway: An integrative cancer interactome analysis.Journal of cellular and molecular medicine · 2022
    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

12 authors at 4 institutions in 2 countries.

Pramod DarvinDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul, South Korea.
Youn Hee JoungDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul, South Korea.
Dong Young KangDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul, South Korea.
Nipin SpDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul, South Korea.
Hyo Joo ByunDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul, South Korea.
Tae Sook HwangDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul, South Korea.
Hema SasidharakurupAmrita School of Biotechnology, Amrita Vishwa Vidyapeetham (Amrita University), Kollam, India.
Chi Ho LeeDepartment of Food Science and Biotechnology of Animal Resources, Konkuk University, Seoul, South Korea.
Kwang Hyun ChoNational Institute of Animal Science, RDA, Cheonan, South Korea.
Kyung Do ParkDepartment of Animal Biotechnology, Chonbuk National University, Jeonju, South Korea.
Hak Kyo LeeDepartment of Animal Biotechnology, Chonbuk National University, Jeonju, South Korea.
Young Mok YangDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul, South Korea.
Konkuk University · KRJeonbuk National University · KRAmrita Vishwa Vidyapeetham · INNational Institute of Animal Science · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tannic acid (TA), a naturally occurring polyphenol, is a potent anti-oxidant with anti-proliferative effects on multiple cancers. However, its ability to modulate gene-specific expression of tumour suppressor genes and oncogenes has not been assessed. This work investigates the mechanism of TA to regulate canonical and non-canonical STAT pathways to impose the gene-specific induction of G1-arrest and apoptosis. Regardless of the p53 status and membrane receptors, TA induced G1-arrest and apoptosis in breast cancer cells. Tannic acid distinctly modulated both canonical and non-canonical STAT pathways, each with a specific role in TA-induced anti-cancer effects. Tannic acid enhanced STAT1 ser727 phosphorylation via upstream serine kinase p38. This STAT1 ser727 phosphorylation enhanced the DNA-binding activity of STAT1 and in turn enhanced expression of p21

Indexed as

ApoptosisBreast NeoplasmsCell Line, TumorCell NucleusCyclin-Dependent Kinase Inhibitor p21Drug SynergismErbB ReceptorsFemaleG1 Phase Cell Cycle CheckpointsGefitinibHumansp38 Mitogen-Activated Protein KinasesPhosphorylationPromoter Regions, GeneticProtein BindingProtein TransportCyclin-Dependent Kinase Inhibitor p21ErbB ReceptorsGefitinibp38 Mitogen-Activated Protein KinasesQuinazolinesSTAT1 Transcription FactorSTAT3 Transcription FactorTamoxifenTanninsG1 arrestp38/STAT1STAT1 ser727STAT3/BCl-2 mitochondrial apoptosistannic acid

Identifiers

PMID27862996
PMCPMC5345631
OpenAlexW2556141906

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.