Evidence map›Paper›PMID 31319814›Full record

ArticleBMC cancer2019

Sirtuin1 activator SRT2183 suppresses glioma cell growth involving activation of endoplasmic reticulum stress pathway.

Tian Ye, Liwen Wei, Ji Shi, Ke Jiang, Huizhe Xu, Lulu Hu, Lingkai Kong, Ye Zhang, Songshu Meng, Haozhe Piao

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.9field-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

20 citing papers in PubMed, 38 citations in OpenAlex.

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  17. Aspirin Induced Glioma Apoptosis through Noxa Upregulation.International journal of molecular sciences · 2020
    Article
  18. Article
  19. The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy.Frontiers in cell and developmental biology · 2020
    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

10 authors at 3 institutions in 1 country.

Tian YeDepartment of Neurosurgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, No. 44 Xiaoheyan Road, Dadong District, Shenyang, 110042, Liaoning Province, China.
Liwen WeiDepartment of Neurosurgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, No. 44 Xiaoheyan Road, Dadong District, Shenyang, 110042, Liaoning Province, China.
Ji ShiDepartment of Neurosurgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, No. 44 Xiaoheyan Road, Dadong District, Shenyang, 110042, Liaoning Province, China.
Ke JiangInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, China.
Huizhe XuInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, China.
Lulu HuInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, China.
Lingkai KongInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, China.
Ye ZhangDepartment of Neurosurgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, No. 44 Xiaoheyan Road, Dadong District, Shenyang, 110042, Liaoning Province, China. zy712@139.com.
Songshu MengInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, China. ssmeng@dmu.edu.cn.
Haozhe PiaoDepartment of Neurosurgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, No. 44 Xiaoheyan Road, Dadong District, Shenyang, 110042, Liaoning Province, China. piaohaozhe@cancerhosp-ln-cmu.com.
Dalian Medical University · CNChina Medical University · CNLiaoning Cancer Hospital & Institute · CN

Funding

National Natural Science Foundation of China 81372471National Natural Science Foundation of China 81572707National Natural Science Foundation of China 81772973Natural Science Foundation of Liaoning Province 20180530059the Development of Local Science and Technology by the Central Government 2017106014the Key Research and Development Project of Liaoning Province 2018225040Young Scientists Fund 81502674
6 · The paper itself

Abstract

backgroundGlioblastoma (GBM) is an extremely deadly form of brain cancer with limited treatment options and thus novel therapeutic modalities are necessary. Histone deacetylase inhibitors (HDACi) have demonstrated clinical and preclinical activities against GBM. (Silent mating type information regulation 2 homolog, Sirt1) abbreviated as Sirtuin 1, has been implicated in GBM. We explored the activity of the Sirt1 activator SRT2183 in glioma cell lines in terms of biological response.

methodsThe effects of SRT2183 on glioma cell growth and neurosphere survival were evaluated in vitro using the CCK-8, clonogenic and neurosphere assays, respectively. Glioma cell cycle arrest and apoptosis were determined by flow cytometry. SRT2183-induced autophagy was investigated by detection of GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3) puncta, conversion of the nonlipidated form of LC3 (LC3-I) to the phosphatidylethanolamine-conjugated form (LC3-II). Acetylation of STAT3 and NF-κB in SRT2183-treated glioma cells was examined using immunoprecipitation. The expression levels of anti-apoptotic proteins were assayed by immunoblotting.

resultsSRT2183 suppressed glioma cell growth and destroyed neurospheres in vitro. Furthermore, SRT2183 induced glioma cell cycle arrest and apoptosis, accompanying by upregulation of the pro-apoptotic Bim and downregulation of Bcl-2 and Bcl-xL. Notably, ER stress was triggered in glioma cells upon exposure to SRT2183 while the pre-exposure to 4-PBA, an ER stress inhibitor, significantly antagonized SRT2183-mediated growth inhibition in glioma cells. In addition, SRT2183 induced autophagy in glioma cells and pharmacological modulation of autophagy appeared not to affect SRT2183-inhibited cell growth. Of interest, the acetylation and phosphorylation of p65 NF-κB and STAT3 in glioma cells were differentially affected by SRT2183.

conclusionsOur data suggest the ER stress pathway is involved in SRT2183-mediated growth inhibition in glioma. Further investigation in vivo is needed to consolidate the data.

Indexed as

AcetylationApoptosisAutophagyBrain NeoplasmsCell Cycle CheckpointsCell Line, TumorCell ProliferationEndoplasmic Reticulum StressGlioblastomaHeterocyclic Compounds, 4 or More RingsHumansHuman Umbilical Vein Endothelial CellsMicrotubule-Associated ProteinsNF-kappa BPhosphorylationSignal TransductionHeterocyclic Compounds, 4 or More RingsMAP1LC3A protein, humanMAP1LC3B protein, humanMicrotubule-Associated ProteinsNF-kappa BSIRT1 protein, humanSirtuin 1SRT2183STAT3 protein, humanSTAT3 Transcription FactorEndoplasmic reticulum stressGliomaNF-κBSirt1STAT3

Identifiers

PMID31319814
PMCPMC6637499
OpenAlexW2959402124

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.