Evidence map›Paper›PMID 25961022›Full record

ArticleBioMed research international2015

{2-[1-(3-Methoxycarbonylmethyl-1H-indol-2-yl)-1-methyl-ethyl]-1H-indol-3-yl}-acetic Acid Methyl Ester Inhibited Hepatocellular Carcinoma Growth in Bel-7402 Cells and Its Resistant Variants by Activation of NOX4 and SIRT3.

Ye Li, Wenjing Wang, Xiaoxue Xu, Shiyue Sun, Xiaoyu Xu, Xian-jun Qu

Abstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Ye LiDepartment of Pharmacology, School of Chemical Biology & Pharmaceutical Sciences, Capital Medical University, Beijing 100069, China.
Wenjing WangDepartment of Medicinal Chemistry, School of Chemical Biology & Pharmaceutical Sciences, Capital Medical University, Beijing 100069, China.
Xiaoxue XuMedical Experiments and Testing Center, Capital Medical University, Beijing 100069, China.
Shiyue SunDepartment of Pharmacology, School of Chemical Biology & Pharmaceutical Sciences, Capital Medical University, Beijing 100069, China.
Xiaoyu XuDepartment of Pharmacology, School of Chemical Biology & Pharmaceutical Sciences, Capital Medical University, Beijing 100069, China.
Xian-jun QuDepartment of Pharmacology, School of Chemical Biology & Pharmaceutical Sciences, Capital Medical University, Beijing 100069, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

{2-[1-(3-Methoxycarbonylmethyl-1H-indol-2-yl)-1-methyl-ethyl]-1H-indol-3-yl}-acetic acid methyl ester (MIAM) is a novel indole compound, which possessed high efficacy against many cancers xenografted in mice without obvious toxicity. In this study, we aimed to investigate the effects of MIAM on human hepatocellular carcinoma (HCC) Bel-7402 cells and its resistant variants Bel-7402/5FU. MIAM inhibited the growth of HCC more potent in Bel-7402/5FU cells than its parent cells. MIAM increased cellular reactive oxygen species (ROS) levels, induced cell apoptosis, and arrested cell cycle in G0/G1 phase. MIAM might exert its action on Bel-7402/5FU cells through activation of NADPH oxidase 4 (NOX4)/p22(phox), Sirtuin3 (SIRT3)/SOD2, and SIRT3/p53/p21(Waf1/Cip) pathways. MIAM might inhibit HCC growth through the modulation of SIRT3. When SIRT3 was silenced, the inhibitory effect of MIAM on Bel-7402/5FU was lowered, showing the characteristic of resistance against MIAM, whereas Bel-7402/5FU cells with high expression of SIRT3 by SIRT3 adenovirus infection demonstrated the high sensitivity to MIAM. These results suggested that MIAM might exert its action against Bel-7402/5FU growth through upregulation of SIRT3. We suggested that MIAM might be a promising candidate compound which could develop as a potent anticancer agent targeting NOX4 and SIRT3 activation.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinoma, HepatocellularCell Cycle CheckpointsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansIndoleacetic AcidsLiver NeoplasmsMiceNADPH Oxidase 4NADPH OxidasesReactive Oxygen SpeciesSirtuin 3(2-(1-(3-methoxycarbonylmethyl-1H-indol-2-yl)-1-methylethyl)-1H-indol-3-yl)acetic acid methyl esterAntineoplastic AgentsIndoleacetic AcidsNADPH Oxidase 4NADPH OxidasesNOX4 protein, humanReactive Oxygen SpeciesSIRT3 protein, humanSirtuin 3

Identifiers

PMID25961022
PMCPMC4413889

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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.