Evidence map›Paper›PMID 26041102›Full record

ArticleScientific reports2015

A new arylbenzofuran derivative functions as an anti-tumour agent by inducing DNA damage and inhibiting PARP activity.

Hongbo Chen, Xiaobin Zeng, Chunmei Gao, Pinghong Ming, Jianping Zhang, Caiping Guo, Lanzhen Zhou, Yin Lu, Lijun Wang, Laiqiang Huang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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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 5 institutions in 1 country.

Hongbo ChenThe Shenzhen Key Lab of Gene and Antibody Therapy, The Ministry-Province Jointly Constructed Base for State Key Lab-Shenzhen Key Laboratory of Chemical Biology, and Division of Life and Health Sciences, Tsinghua University Shenzhen Graduate School, Shenzhen 518055, China; School of Life Sciences, Tsinghua University, Beijing 100084, China.
Xiaobin Zeng1] The Shenzhen Key Lab of Gene and Antibody Therapy, The Ministry-Province Jointly Constructed Base for State Key Lab-Shenzhen Key Laboratory of Chemical Biology, and Division of Life and Health Sciences, Tsinghua University Shenzhen Graduate School, Shenzhen 518055, China; School of Life Sciences, Tsinghua University, Beijing 100084, China [2] Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical College, Zhanjiang 524023, Guangdong, China.
Chunmei GaoThe Shenzhen Key Lab of Gene and Antibody Therapy, The Ministry-Province Jointly Constructed Base for State Key Lab-Shenzhen Key Laboratory of Chemical Biology, and Division of Life and Health Sciences, Tsinghua University Shenzhen Graduate School, Shenzhen 518055, China; School of Life Sciences, Tsinghua University, Beijing 100084, China.
Pinghong MingClinical laboratory, Zhuhai People's hospital, Zhuhai 519000, China.
Jianping ZhangShenzhen Weiguang Biological Products Co., Ltd, Shenzhen 518107, China.
Caiping GuoShenzhen Weiguang Biological Products Co., Ltd, Shenzhen 518107, China.
Lanzhen ZhouShenzhen Weiguang Biological Products Co., Ltd, Shenzhen 518107, China.
Yin LuDrug Discovery and Design Center (DDDC), Shanghai Institute of Materia Medica, Shanghai 201203, China.
Lijun WangThe Shenzhen Key Lab of Gene and Antibody Therapy, The Ministry-Province Jointly Constructed Base for State Key Lab-Shenzhen Key Laboratory of Chemical Biology, and Division of Life and Health Sciences, Tsinghua University Shenzhen Graduate School, Shenzhen 518055, China; School of Life Sciences, Tsinghua University, Beijing 100084, China.
Laiqiang HuangThe Shenzhen Key Lab of Gene and Antibody Therapy, The Ministry-Province Jointly Constructed Base for State Key Lab-Shenzhen Key Laboratory of Chemical Biology, and Division of Life and Health Sciences, Tsinghua University Shenzhen Graduate School, Shenzhen 518055, China; School of Life Sciences, Tsinghua University, Beijing 100084, China.
Xiangjiu HeCollege of Pharmacy, Guangdong Pharmaceutical University, Guangzhou 510006, China.
Lin MeiThe Shenzhen Key Lab of Gene and Antibody Therapy, The Ministry-Province Jointly Constructed Base for State Key Lab-Shenzhen Key Laboratory of Chemical Biology, and Division of Life and Health Sciences, Tsinghua University Shenzhen Graduate School, Shenzhen 518055, China; School of Life Sciences, Tsinghua University, Beijing 100084, China.
Tsinghua University · CNShenzhen Weiguang Biological Products (China) · CNGuangdong Pharmaceutical University · CNShanghai Institute of Materia Medica · CNZhuhai People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that 7-hydroxy-5, 4'-dimethoxy-2-arylbenzofuran (HDAB) purified from Livistona chinensis is a key active agent. The present study investigated the function and molecular mechanism of HDAB. HDAB treatment of cervical cancer cells resulted in S phase arrest and apoptosis, together with cyclin A2 and CDK2 upregulation. Cyclin A2 siRNA and a CDK inhibitor efficiently relieved S phase arrest but increased the apoptosis rate. Mechanistic studies revealed that HDAB treatment significantly increased DNA strand breaks in an alkaline comet assay and induced ATM, CHK1, CHK2 and H2A.X phosphorylation. Wortmannin (a broad inhibitor of PIKKs) and CGK733 (a specific ATM inhibitor), but not LY294002 (a phosphatidylinositol 3-kinase inhibitor) or NU7026 (a DNA-PK specific inhibitor), prevented H2A.X phosphorylation and γH2A.X-positive foci formation in the nuclei, reversed S phase arrest and promoted the HDAB-induced apoptosis, suggesting that HDAB is a DNA damaging agent that can activate the ATM-dependent DNA repair response, thereby contributing to cell cycle arrest. In addition, molecular docking and in vitro activity assays revealed that HDAB can correctly dock into the hydrophobic pocket of PARP-1 and suppress PARP-1 ADP-ribosylation activity. Thus, the results indicated that HDAB can function as an anti-cancer agent by inducing DNA damage and inhibiting PARP activity.

Indexed as

Antineoplastic Agents, PhytogenicApoptosisBenzofuransCell Line, TumorCell ProliferationCyclin A2Cyclin-Dependent Kinase 2DNA DamageDNA RepairHumansModels, MolecularMolecular ConformationPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesProtein BindingS Phase Cell Cycle CheckpointsAntineoplastic Agents, PhytogenicBenzofuransCyclin A2Cyclin-Dependent Kinase 2Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerases

Identifiers

PMID26041102
PMCPMC4455115
OpenAlexW2260774729

What OpenQuestion holds

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LicenceCC BY
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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.