Evidence map›Paper›PMID 27995497›Full record

ArticleNeurochemical research2017

Induction of G1 Cell Cycle Arrest in Human Glioma Cells by Salinomycin Through Triggering ROS-Mediated DNA Damage In Vitro and In Vivo.

Shi-Jun Zhao, Xian-Jun Wang, Qing-Jian Wu, Chao Liu, Da-Wei Li, Xiao-Ting Fu, Hui-Fang Zhang, Lu-Rong Shao, Jing-Yi Sun, Bao-Liang Sun and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2017. 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
1.7field-weighted citation impact, top 13% 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, 33 citations in OpenAlex.

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  14. Combined Strategy of RadioactiveNeurochemical research · 2018
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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 3 institutions in 1 country.

Shi-Jun ZhaoDepartment of Neurology, Shandong University School of Medicine, Jinan, Shandong, 250012, China.
Xian-Jun WangDepartment of Neurology, Linyi People's Hospital, Linyi, Shandong, 276000, China.
Qing-Jian WuTaishan Medical University, Taian, Shandong, 271000, China.
Chao LiuTaishan Medical University, Taian, Shandong, 271000, China.
Da-Wei LiTaishan Medical University, Taian, Shandong, 271000, China.
Xiao-Ting FuTaishan Medical University, Taian, Shandong, 271000, China.
Hui-Fang ZhangTaishan Medical University, Taian, Shandong, 271000, China.
Lu-Rong ShaoTaishan Medical University, Taian, Shandong, 271000, China.
Jing-Yi SunTaishan Medical University, Taian, Shandong, 271000, China.
Bao-Liang SunTaishan Medical University, Taian, Shandong, 271000, China. blsun88@163.com.
Jing ZhaiTaishan Medical University, Taian, Shandong, 271000, China. jingzhai66@163.com.
Cun-Dong FanTaishan Medical University, Taian, Shandong, 271000, China. tcdfan66@163.com.
Taishan Medical University · CNBaotou Central Hospital · CNLinyi People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy has always been one of the most effective ways in combating human glioma. However, the high metastatic potential and resistance toward standard chemotherapy severely hindered the chemotherapy outcomes. Hence, searching effective chemotherapy drugs and clarifying its mechanism are of great significance. Salinomycin an antibiotic shows novel anticancer potential against several human tumors, including human glioma, but its mechanism against human glioma cells has not been fully elucidated. In the present study, we demonstrated that salinomycin treatment time- and dose-dependently inhibited U251 and U87 cells growth. Mechanically, salinomycin-induced cell growth inhibition against human glioma was mainly achieved by induction of G1-phase arrest via triggering reactive oxide species (ROS)-mediated DNA damage, as convinced by the activation of histone, p53, p21 and p27. Furthermore, inhibition of ROS accumulation effectively attenuated salinomycin-induced DNA damage and G1 cell cycle arrest, and eventually reversed salinomycin-induced cytotoxicity. Importantly, salinomycin treatment also significantly inhibited the U251 tumor xenograft growth in vivo through triggering DNA damage-mediated cell cycle arrest with involvement of inhibiting cell proliferation and angiogenesis. The results above validated the potential of salinomycin-based chemotherapy against human glioma.

Indexed as

AnimalsCell Line, TumorCell SurvivalDNA DamageDose-Response Relationship, DrugG1 Phase Cell Cycle CheckpointsGliomaHumansMaleMiceMice, NudePolyether PolyketidesPyransReactive Oxygen SpeciesXenograft Model Antitumor AssaysPolyether PolyketidesPyransReactive Oxygen SpeciessalinomycinCell cycle arrestDNA damageGliomaReactive oxide speciesSalinomycin

Identifiers

PMID27995497
OpenAlexW2567527235

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.