Evidence map›Paper›PMID 29849127›Full record

ArticleActa pharmacologica Sinica2018

Escin-induced DNA damage promotes escin-induced apoptosis in human colorectal cancer cells via p62 regulation of the ATM/γH2AX pathway.

Zhong Wang, Qiang Chen, Bin Li, Jia-Ming Xie, Xiao-Dong Yang, Kui Zhao, Yong Wu, Zhen-Yu Ye, Zheng-Rong Chen, Zheng-Hong Qin and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 34 citations in OpenAlex.

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  13. Theasaponin EMolecules (Basel, Switzerland) · 2021
    Article
  14. Review
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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

11 authors at 3 institutions in 1 country.

Zhong WangDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215007, China.
Qiang ChenDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215007, China.
Bin LiDepartment of General Surgery, the First People's Hospital of Wu Jiang, Suzhou, 215200, China.
Jia-Ming XieDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215007, China.
Xiao-Dong YangDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215007, China.
Kui ZhaoDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215007, China.
Yong WuDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215007, China.
Zhen-Yu YeDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215007, China.
Zheng-Rong ChenDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215007, China.
Zheng-Hong QinDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, College of Pharmaceutical Science, Soochow University, Suzhou, 215123, China. qinzhenhong@suda.edu.cn.
Chun-Gen XingDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215007, China. xingcgchn@163.com.
Soochow University · CNSecond Affiliated Hospital of Soochow University · CNThe First People's Hospital of Jiangxia District · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Escin, a triterpene saponin isolated from horse chestnut seed, has been used to treat encephaledema, tissue swelling and chronic venous insufficiency. Recent studies show that escin induces cell cycle arrest, tumor proliferation inhibition and tumor cell apoptosis. But the relationship between escin-induced DNA damage and cell apoptosis in tumor cells remains unclear. In this study, we investigated whether and how escin-induced DNA damage contributed to escin-induced apoptosis in human colorectal cancer cells. Escin (5-80 μg/mL) dose-dependently inhibited the cell viability and colony formation in HCT116 and HCT8 cells. Escin treatment induced DNA damage, leading to p-ATM and γH2AX upregulation. Meanwhile, escin treatment increased the expression of p62, an adaptor protein, which played a crucial role in controlling cell survival and tumorigenesis, and had a protective effect against escin-induced DNA damage: knockdown of p62 apparently enhanced escin-induced DNA damage, whereas overexpression of p62 reduced escin-induced DNA damage. In addition, escin treatment induced concentration- and time-dependent apoptosis. Similarly, knockdown of p62 significantly increased escin-induced apoptosis in vitro and produced en escin-like antitumor effect in vivo. Overexpression of p62 decreased the rate of apoptosis. Further studies revealed that the functions of p62 in escin-induced DNA damage were associated with escin-induced apoptosis, and p62 knockdown combined with the ATM inhibitor KU55933 augmented escin-induced DNA damage and further increased escin-induced apoptosis. In conclusion, our results demonstrate that p62 regulates ATM/γH2AX pathway-mediated escin-induced DNA damage and apoptosis.

Indexed as

AnimalsAntineoplastic AgentsApoptosisAtaxia Telangiectasia Mutated ProteinsAutophagyCell Line, TumorCell ProliferationColorectal NeoplasmsDNA DamageDown-RegulationEscinFemaleHistonesHumansMice, NudeSequestosome-1 ProteinAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsATM protein, humanEscinH2AX protein, humanHistonesSequestosome-1 ProteinSQSTM1 protein, humanapoptosis, colorectal cancerescin, p62, DNA damage, ATM/γH2AX pathwayHCT116 cellsHCT8 cells

Identifiers

PMID29849127
PMCPMC6289333
OpenAlexW2806566403

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.