Evidence map›Paper›PMID 26846141›Full record

ArticleNeurochemical research2016

Induction of S-Phase Arrest in Human Glioma Cells by Selenocysteine, a Natural Selenium-Containing Agent Via Triggering Reactive Oxygen Species-Mediated DNA Damage and Modulating MAPKs and AKT Pathways.

Kun Wang, Xiao-Ting Fu, Yuan Li, Ya-Jun Hou, Ming-Feng Yang, Jing-Yi Sun, Shu-Ying Yi, Cun-Dong Fan, Xiao-Yan Fu, Jing Zhai and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2016. 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
3.2field-weighted citation impact, top 9% 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, 28 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

11 authors at 3 institutions in 1 country.

Kun WangDepartment of Neurology, Shandong University School of Medicine, Jinan, 250012, Shandong, China.
Xiao-Ting FuKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000, Shandong, China.
Yuan LiKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000, Shandong, China.
Ya-Jun HouKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000, Shandong, China.
Ming-Feng YangKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000, Shandong, China.
Jing-Yi SunSchool of Basic Medicine, Taishan Medical University, Taian, 271000, Shandong, China.
Shu-Ying YiSchool of Basic Medicine, Taishan Medical University, Taian, 271000, Shandong, China.
Cun-Dong FanKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000, Shandong, China. tcdfan66@163.com.
Xiao-Yan FuSchool of Basic Medicine, Taishan Medical University, Taian, 271000, Shandong, China. fxy007800@163.com.
Jing ZhaiSchool of Basic Medicine, Taishan Medical University, Taian, 271000, Shandong, China. jingzhai66@163.com.
Bao-Liang SunKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000, Shandong, China. blsun88@163.com.
Taishan Medical University · CNAffiliated Hospital of Taishan Medical University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Selenocysteine (SeC) a natural available selenoamino acid exhibits novel anticancer activities against human cancer cell lines. However, the growth inhibitory effect and mechanism of SeC in human glioma cells remain unclear. The present study reveals that SeC time- and dose-dependently inhibited U251 and U87 human glioma cells growth by induction of S-phase cell cycle arrest, followed by the marked decrease of cyclin A. SeC-induced S-phase arrest was achieved by inducing DNA damage through triggering generation of reactive oxygen species (ROS) and superoxide anion, with concomitant increase of TUNEL-positive cells and induction of p21waf1/Cip1 and p53. SeC treatment also caused the activation of p38MAPK, JNK and ERK, and inactivation of AKT. Four inhibitors of MAPKs and AKT pathways further confirmed their roles in SeC-induced S-phase arrest in human glioma cells. Our findings advance the understanding on the molecular mechanisms of SeC in human glioma management.

Indexed as

Antineoplastic AgentsCell Cycle CheckpointsCell Line, TumorCell SurvivalDNA DamageGliomaHumansMAP Kinase Signaling SystemOncogene Protein v-aktReactive Oxygen SpeciesSeleniumSelenocysteineAntineoplastic AgentsOncogene Protein v-aktReactive Oxygen SpeciesSeleniumSelenocysteineAKTCell cycle arrestDNA damageGliomaMAPKsReactive oxygen speciesSelenocysteine

Identifiers

PMID26846141
OpenAlexW2262901860

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.