Evidence map›Paper›PMID 28360085›Full record

ArticleBone & joint research2017

Silencing of translation initiation factor eIF3b promotes apoptosis in osteosarcoma cells.

Y J Choi, Y S Lee, H W Lee, D M Shim, S W Seo

Open access · goldAbstract read
In one paragraph

Article in Bone & joint research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 35 citations in OpenAlex.

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  12. Role of RONS and eIFs in Cancer Progression.Oxidative medicine and cellular longevity · 2021
    Review
  13. Eukaryotic translation initiation factor 3 subunit b is a novel oncogenic factor in prostate cancer.Mammalian genome : official journal of the International Mammalian Genome Society · 2020
    Article
  14. Article
  15. Article
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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

5 authors at 2 institutions in 1 country.

Y J ChoiDepartment of Orthopaedic Surgery, Samsung Medical Center, Sungkyunkwan University, 50, Ilwon-dong, Gangnam-gu, 135-710, Seoul, South Korea.
Y S LeeDepartment of Orthopaedic Surgery, Samsung Medical Center, Sungkyunkwan University, 50, Ilwon-dong, Gangnam-gu, 135-710, Seoul, South Korea.
H W LeeDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, 50, Ilwon-dong, Gangnam-gu, 135-710, Seoul, South Korea.
D M ShimDepartment of Orthopaedic Surgery, Samsung Medical Center, Sungkyunkwan University, 50, Ilwon-dong, Gangnam-gu, 135-710, Seoul, South Korea.
S W SeoDepartment of Orthopaedic Surgery, Samsung Medical Center, Sungkyunkwan University, 50, Ilwon-dong, Gangnam-gu, 135-710, Seoul, South Korea sungwseo@gmail.com.
Sungkyunkwan University · KRSamsung Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesEukaryotic translation initiation factor 3 (eIF3) is a multi-subunit complex that plays a critical role in translation initiation. Expression levels of eIF3 subunits are elevated or decreased in various cancers, suggesting a role for eIF3 in tumorigenesis. Recent studies have shown that the expression of the eIF3b subunit is elevated in bladder and prostate cancer, and eIF3b silencing inhibited glioblastoma growth and induced cellular apoptosis. In this study, we investigated the role of eIF3b in the survival of osteosarcoma cells.

methodsTo investigate the effect of eIF3b on cell viability and apoptosis in osteosarcoma cells, we first examined the silencing effect of eIF3b in U2OS cells. Cell viability and apoptosis were examined by the Cell Counting Kit-8 (CCK-8) assay and Western blot, respectively. We also performed gene profiling to identify genes affected by eIF3b silencing. Finally, the effect of eIF3b on cell viability and apoptosis was confirmed in multiple osteosarcoma cell lines.

resultseIF3b silencing decreased cell viability and induced apoptosis in U2OS cells, and by using gene profiling we discovered that eIF3b silencing also resulted in the upregulation of tumour necrosis factor receptor superfamily member 21 (TNFRSF21). We found that TNFRSF21 overexpression induced cell death in U2OS cells, and we confirmed that eIF3b silencing completely suppressed cell growth in multiple osteosarcoma cell lines. However, eIF3b silencing failed to suppress cell growth completely in normal fibroblast cells.

conclusionOur data led us to conclude that eIF3b may be required for osteosarcoma cell proliferation by regulating TNFRSF21 expression.

Indexed as

ApoptosiseIF3bOsteosarcomaTNFRSF21Translation

Identifiers

PMID28360085
PMCPMC5376660
OpenAlexW2604071896

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.