Evidence map›Paper›PMID 36071872›Full record

ArticleOxidative medicine and cellular longevity2022

EID3 Promotes Cancer Stem Cell-Like Phenotypes in Osteosarcoma through the Activation of PI3K-AKT Signaling Pathway.

Yan Wang, Shiyong Luo, Yuxuan Wang, Shengbang Yang, Zhitong Huang, Xuejin Zhu, Shanghua Cai, Qifeng Guo, Weide Zhong, Sihong Liu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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 2 institutions in 1 country.

Yan WangDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong 510180, China.ORCID https://orcid.org/0000-0002-1490-7450
Shiyong LuoDepartment of Orthopedics, Guangzhou First People's Hospital, Guangzhou Guangdong 510182, China.
Yuxuan WangDepartment of Orthopedics, The Second People's Hospital of Panyu, Guangzhou, Guangdong 510182, China.
Shengbang YangDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong 510180, China.
Zhitong HuangDepartment of Orthopedics, Guangzhou First People's Hospital, Guangzhou Guangdong 510182, China.
Xuejin ZhuDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong 510180, China.ORCID https://orcid.org/0000-0001-6251-1197
Shanghua CaiDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong 510180, China.
Qifeng GuoDepartment of Orthopedics, Guangzhou First People's Hospital, Guangzhou Guangdong 510182, China.ORCID https://orcid.org/0000-0003-3818-0716
Weide ZhongDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong 510180, China.ORCID https://orcid.org/0000-0002-0430-2845
Sihong LiuDepartment of Orthopedics, Guangzhou First People's Hospital, Guangzhou Guangdong 510182, China.ORCID https://orcid.org/0000-0003-4588-2468
Guangzhou First People's Hospital · CNPanyu Hospital of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study is to elucidate molecular mechanism by which E1A-like inhibitor of differentiation 3 (EID3) promotes cancer stem cell-like phenotypes in osteosarcoma. Overexpression of EID3 in osteosarcoma cells generated more spherical clones, enhanced the expression of stemness-associated genes, and promoted chemoresistance, invasion, and metastasis. Furthermore, osteosarcoma cells overexpressing EID3 had increased ability to grow in suspension as osteospheres with high expression of Sox2 and stem cell marker CD133. In addition, knockdown of EID3 reduced sphere formation and inhibited osteosarcoma cell migration and invasion. RNA sequencing and bioinformatics analysis revealed that PI3K-Akt signaling pathway and MAPK pathway-related genes were enriched in osteosarcoma cells with high expression of EID3. Taken together, EID3 promotes osteosarcoma, and EID3-PI3K-Akt axis is a potential therapeutic target for osteosarcoma treatment.

Indexed as

Bone NeoplasmsCarrier ProteinsNeoplastic Stem CellsOsteosarcomaCell Line, TumorGene Expression Regulation, NeoplasticHumansPhenotypePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCarrier ProteinsEID3 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID36071872
PMCPMC9441394
OpenAlexW4293390691

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.