Evidence map›Paper›PMID 27082635›Full record

ArticleInternational journal of oncology2016

Theaflavin-3, 3'-digallate induces apoptosis and G2 cell cycle arrest through the Akt/MDM2/p53 pathway in cisplatin-resistant ovarian cancer A2780/CP70 cells.

Youying Tu, Eunhye Kim, Ying Gao, Gary O Rankin, Bo Li, Yi Charlie Chen

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
5.9field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  16. Anti-Cancer Properties of Theaflavins.Molecules (Basel, Switzerland) · 2021
    Review
  17. Theaflavin Chemistry and Its Health Benefits.Oxidative medicine and cellular longevity · 2021
    Review
  18. Article
  19. Article
  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

6 authors at 2 institutions in 2 countries.

Youying TuDepartment of Tea Science, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.
Eunhye KimDepartment of Tea Science, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.
Ying GaoDepartment of Tea Science, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.
Gary O RankinDepartment of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA.
Bo LiDepartment of Tea Science, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.
Yi Charlie ChenDepartment of Tea Science, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.
Zhejiang University · CNMarshall University · US

Funding

WV INBRE: The Inhibitor of Growth Family Member 4 (ING4) inhibits L-Type Amino Acid Transporter 1 (LAT1) expression to suppress Breast CancerP20GM103434 · NIGMS · MARSHALL UNIVERSITY · PI GARY O RANKIN · 2012 to 2026
$61.1M
WVU &MU NEW FACULTY GRANTSP20RR016477 · NCRR · MARSHALL UNIVERSITY · PI RANKIN, GARY O · 2001 to 2011
$35.5M
NCRR NIH HHS P20 RR016477NIGMS NIH HHS P20 GM103434
6 · The paper itself

Abstract

Ovarian cancer is the most lethal gynecological cancer among women worldwide. Adverse side effects and acquired resistance to conventional platinum based chemotherapy are major impediments in ovarian cancer treatment, and drive the development of more selective anticancer drugs that target cancer-specific defects. In this study, theaflavin-3, 3'-digallate (TF3), the major theaflavin monomer in black tea, exhibited a potent growth inhibitory effect on the cisplatin-resistant ovarian cancer A2780/CP70 cells (IC50, 23.81 µM), and was less cytotoxic to a normal ovarian IOSE‑364 cells (IC50, 59.58 µM) than to the cancer cells. Flow cytometry analysis indicated that TF3 induced preferential apoptosis and G2 cell cycle arrest in A2780/CP70 cells with respect to IOSE‑364 cells. TF3 induced apoptosis through both the intrinsic and extrinsic apoptotic pathways, and caused G2 cell cycle arrest via cyclin B1 in A2780/CP70 cells. The p53 protein played an important role in TF3-induced apoptosis and G2 cell cycle arrest. TF3 might upregulate the p53 expression via the Akt/MDM2 pathway. Our findings help elucidate the mechanisms by which TF3 may contribute to the prevention and treatment of platinum-resistant ovarian cancer.

Indexed as

ApoptosisBiflavonoidsCatechinCell Line, TumorCell ProliferationCell SurvivalCisplatinDrug Resistance, NeoplasmFemaleG2 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansOvarian NeoplasmsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mdm2Signal TransductionBiflavonoidsCatechinCisplatinMDM2 protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mdm2theaflavin-3,3'-digallateTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID27082635
PMCPMC4863729
OpenAlexW2316528037

What OpenQuestion holds

Textmetadata
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.