Evidence map›Paper›PMID 38692271›Full record

ArticleCell reports. Medicine2024

Tumor mitochondrial oxidative phosphorylation stimulated by the nuclear receptor RORγ represents an effective therapeutic opportunity in osteosarcoma.

Jianwei Zheng, Qianqian Wang, Jianghe Chen, Guodi Cai, Zhenhua Zhang, Hongye Zou, June X Zou, Qianqian Liu, Shufeng Ji, Guoli Shao and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports. Medicine, 2024. 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
4.6field-weighted citation impact, top 5% 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, 16 citations in OpenAlex.

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  14. Spatial Transcriptomics Advances the Use of Canine Patients in Cancer Research: Analysis of Osteosarcoma-Bearing Pet Dogs Enrolled in a Clinical Trial.Clinical cancer research : an official journal of the American Association for Cancer 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

17 authors at 4 institutions in 3 countries.

Jianwei ZhengSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China.
Qianqian WangSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China.
Jianghe ChenSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China.
Guodi CaiSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China.
Zhenhua ZhangSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China.
Hongye ZouDepartment of Biochemistry and Molecular Medicine, UC Davis Comprehensive Cancer Center, School of Medicine, University of California, Davis, Sacramento, CA, USA.
June X ZouDepartment of Biochemistry and Molecular Medicine, UC Davis Comprehensive Cancer Center, School of Medicine, University of California, Davis, Sacramento, CA, USA.
Qianqian LiuSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China.
Shufeng JiSpecial Medical Service Center, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Guoli ShaoSpecial Medical Service Center, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Hong LiBiomedical Laboratory, Guangzhou Jingke Life Science Institute, Guangzhou, Guangdong 510145, P.R. China.
Sheng LiBiomedical Laboratory, Guangzhou Jingke Life Science Institute, Guangzhou, Guangdong 510145, P.R. China.
Hong-Wu ChenDepartment of Biochemistry and Molecular Medicine, UC Davis Comprehensive Cancer Center, School of Medicine, University of California, Davis, Sacramento, CA, USA.
LinLin LuJoint Laboratory for Translational Cancer Research of Chinese Medicine of the Ministry of Education of the People's Republic of China, International Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, China; State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, SAR, China.
Yanqiu YuanSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China. Electronic address: yuanyq8@mail.sysu.edu.cn.
Peiqing LiuSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China; National-Local Joint Engineering Laboratory of Druggability and New Drugs Evaluation, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China; Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China. Electronic address: liupq@mail.sysu.edu.cn.
Junjian WangSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China; National-Local Joint Engineering Laboratory of Druggability and New Drugs Evaluation, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China; Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, P.R. China. Electronic address: wangjj87@mail.sysu.edu.cn.
Sun Yat-sen University · CNUC Davis Comprehensive Cancer CenterZhujiang Hospital · CNMacau University of Science and Technology · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma (OS) is the most common malignant bone tumor with a poor prognosis. Here, we show that the nuclear receptor RORγ may serve as a potential therapeutic target in OS. OS exhibits a hyperactivated oxidative phosphorylation (OXPHOS) program, which fuels the carbon source to promote tumor progression. We found that RORγ is overexpressed in OS tumors and is linked to hyperactivated OXPHOS. RORγ induces the expression of PGC-1β and physically interacts with it to activate the OXPHOS program by upregulating the expression of respiratory chain component genes. Inhibition of RORγ strongly inhibits OXPHOS activation, downregulates mitochondrial functions, and increases ROS production, which results in OS cell apoptosis and ferroptosis. RORγ inverse agonists strongly suppressed OS tumor growth and progression and sensitized OS tumors to chemotherapy. Taken together, our results indicate that RORγ is a critical regulator of the OXPHOS program in OS and provides an effective therapeutic strategy for this deadly disease.

Indexed as

Bone NeoplasmsMitochondriaNuclear Receptor Subfamily 1, Group F, Member 3OsteosarcomaOxidative PhosphorylationAnimalsApoptosisCell Line, TumorCell ProliferationFerroptosisGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeReactive Oxygen SpeciesNuclear Receptor Subfamily 1, Group F, Member 3PPARGC1B protein, humanReactive Oxygen SpeciesRNA-Binding Proteins

Identifiers

PMID38692271
PMCPMC11148566
OpenAlexW4396520296

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.