Evidence map›Paper›PMID 35918761›Full record

ArticleJournal of translational medicine2022

IGF2BP1-regulated expression of ERRα is involved in metabolic reprogramming of chemotherapy resistant osteosarcoma cells.

Qing He, Peng Hao, Gang He, Hantao Mai, Wenzhou Liu, Weiqiong Zhang, Kelin Zhang, Guifang Zhong, Ruilian Guo, Changzhi Yu and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Ferroptosis Suppression by the MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  7. mActa pharmaceutica Sinica. B · 2025
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  10. Abnormal changes in metabolites caused by mJournal of advanced research · 2025
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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

14 authors at 2 institutions in 1 country.

Qing HeDepartment of Surgical Intensive Care Unit, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Peng HaoDepartment of Surgical Intensive Care Unit, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Gang HeDepartment of Orthopedics, Guangzhou Zengcheng District People's Hospital, Guangzhou, China.
Hantao MaiDepartment of Surgical Intensive Care Unit, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Wenzhou LiuDepartment of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, No.107, Yanjiang West Road, Yuexiu, Guangzhou, 510120, China.
Weiqiong ZhangDepartment of Orthopedics, Guangzhou Zengcheng District People's Hospital, Guangzhou, China.
Kelin ZhangDepartment of Surgical Intensive Care Unit, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Guifang ZhongDepartment of Surgical Intensive Care Unit, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Ruilian GuoDepartment of Surgical Intensive Care Unit, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Changzhi YuDepartment of Chinese Traditional Medicine, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Yang LiPediatric Hematology & Oncology, Sun Yat-sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Chipiu WongDepartment of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, No.107, Yanjiang West Road, Yuexiu, Guangzhou, 510120, China.
Qian ChenDepartment of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, No.107, Yanjiang West Road, Yuexiu, Guangzhou, 510120, China.
Yantao ChenDepartment of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, No.107, Yanjiang West Road, Yuexiu, Guangzhou, 510120, China. chenyant@mail.sysu.edu.cn.
Sun Yat-sen Memorial Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin (Dox) is the standard treatment approach for osteosarcoma (OS), while acquired drug resistance seriously attenuates its treatment efficiency. The present study aimed to investigate the potential roles of metabolic reprogramming and the related regulatory mechanism in Dox-resistant OS cells. The results showed that the ATP levels, lactate generation, glucose consumption and oxygen consumption rate were significantly increased in Dox-resistant OS cells compared with parental cells. Furthermore, the results revealed that the increased expression of estrogen-related receptor alpha (ERRα) was involved in metabolic reprogramming in chemotherapy resistant OS cells, since targeted inhibition of ERRα restored the shifting of metabolic profiles. Mechanistic analysis indicated that the mRNA stability, rather than ERRα transcription was markedly increased in chemoresistant OS cells. Therefore, it was hypothesized that the 3'-untranslated region of ERRα mRNA was methylated by N

Indexed as

Bone NeoplasmsOsteosarcoma3' Untranslated RegionsCell Line, TumorDoxorubicinDrug Resistance, NeoplasmERRalpha Estrogen-Related ReceptorHumansReceptors, Estrogen3' Untranslated RegionsDoxorubicinERRalpha Estrogen-Related ReceptorReceptors, EstrogenDoxorubicinEstrogen-related receptor alphaInsulin-like growth factor 2 mRNA binding protein 1N6‑methyladenineOsteosarcoma

Identifiers

PMID35918761
PMCPMC9344706
OpenAlexW4289785799

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.