Evidence map›Paper›PMID 26801633›Full record

ArticleAntioxidants & redox signaling2016

Epigenetic Upregulation of Metallothionein 2A by Diallyl Trisulfide Enhances Chemosensitivity of Human Gastric Cancer Cells to Docetaxel Through Attenuating NF-κB Activation.

Yuanming Pan, Shuye Lin, Rui Xing, Min Zhu, Bonan Lin, Jiantao Cui, Wenmei Li, Jing Gao, Lin Shen, Yuanyuan Zhao and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
14.4field-weighted citation impact, top 2% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

  1. Effects ofBMJ (Clinical research ed.) · 2019
    Trial
  2. Article
  3. Coordinated DNA 5-mC and RNA mExperimental & molecular medicine · 2026
    Article
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  17. Canadian journal of gastroenterology & hepatology · 2022
    Article
  18. Review
  19. DifferentialOncology reports · 2021
    Observational
  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

14 authors at 6 institutions in 2 countries.

Yuanming Pan1 Laboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital/Institute , Beijing, P.R. China .
Shuye Lin2 College of Life Sciences and Bioengineering, School of Science, Beijing Jiaotong University, 3 Shangyuancun, Haidian District, Beijing, P.R. China .
Rui Xing1 Laboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital/Institute , Beijing, P.R. China .
Min Zhu1 Laboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital/Institute , Beijing, P.R. China .
Bonan Lin2 College of Life Sciences and Bioengineering, School of Science, Beijing Jiaotong University, 3 Shangyuancun, Haidian District, Beijing, P.R. China .
Jiantao Cui1 Laboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital/Institute , Beijing, P.R. China .
Wenmei Li1 Laboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital/Institute , Beijing, P.R. China .
Jing Gao4 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of GI Oncology, Peking University School of Oncology , Peking Cancer Hospital, Beijing, P.R. China .
Lin Shen4 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of GI Oncology, Peking University School of Oncology , Peking Cancer Hospital, Beijing, P.R. China .
Yuanyuan Zhao5 CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, National Center for Nanoscience and Technology of China , Beijing, P.R. China .
Mingzhou Guo6 Department of Gastroenterology and Hepatology, Chinese PLA General Hospital , Beijing, P.R. China .
Ji Ming Wang3 Laboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland.
Jiaqiang Huang2 College of Life Sciences and Bioengineering, School of Science, Beijing Jiaotong University, 3 Shangyuancun, Haidian District, Beijing, P.R. China .
Youyong Lu1 Laboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital/Institute , Beijing, P.R. China .
Peking University Cancer Hospital · CNNational Cancer Institute · USPeking University · CNChinese PLA General Hospital · CNFrederick National Laboratory for Cancer Research · USNational Center for Nanoscience and Technology · CN

Funding

Role of Formylpeptide Receptors in Host DefenseZIABC010725 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, JI MING · 2009 to 2023
$6.3M
NCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

aimsMetallothionein 2A (MT2A) and nuclear factor-kappaB (NF-κB) are both involved in carcinogenesis and cancer chemosensitivity. We previously showed decreased expression of MT2A and IκB-α in human gastric cancer (GC) associated with poor prognosis of GC patients. The present study investigated the effect of diallyl trisulfide (DATS), a garlic-derived compound, and docetaxel (DOC) on regulation of MT2A in relation to NF-κB in GC cells.

resultsDATS attenuated NF-κB signaling in GC cells, resulting in G2/M cell cycle arrest and apoptosis, culminating in the inhibition of cell proliferation and tumorigenesis in nude mice. The anti-GC effect of DATS was attributable to its capacity to epigenetically upregulate MT2A, which in turn enhanced transcription of IκB-α to suppress NF-κB activation in GC cells. The combination of DATS with DOC exhibited a synergistic anti-GC activity accompanied by MT2A upregulation and NF-κB inactivation. Histopathologic analysis of GC specimens from patients showed a significant increase in MT2A expression following DOC treatment. GC patients with high MT2A expression in tumor specimens showed significantly improved response to chemotherapy and prolonged survival compared with those with low MT2A expression in tumors. INNOVATION AND

conclusionWe conclude that DATS exerts its anti-GC activity and enhances chemosensitivity of GC to DOC by epigenetic upregulation of MT2A to attenuate NF-κB signaling. Our findings delineate a mechanistic basis of MT2A/NF-κB signaling for DATS- and DOC-mediated anti-GC effects, suggesting that MT2A may be a chemosensitivity indicator in GC patients receiving DOC-based treatment and a promising target for more effective treatment of GC by combination of DATS and DOC. Antioxid. Redox Signal. 24, 839-854.

Indexed as

AdultAgedAllyl CompoundsAnimalsAntineoplastic AgentsApoptosisBiomarkers, TumorCell Cycle CheckpointsCell Line, TumorCell ProliferationDocetaxelDrug Resistance, NeoplasmDrug SynergismEpigenesis, GeneticFemaleGene ExpressionAllyl CompoundsAntineoplastic AgentsBiomarkers, Tumordiallyl trisulfideDocetaxelMetallothioneinMT2A protein, humanNF-kappa BSulfidesTaxoids

Identifiers

PMID26801633
PMCPMC4876530
OpenAlexW2327837206

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.