Evidence map›Paper›PMID 38191316›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Soy isoflavones induces mitophagy to inhibit the progression of osteosarcoma by blocking the AKT/mTOR signaling pathway.

Ziang Zheng, Xinghan Zhao, Bo Yuan, Shan Jiang, Rushan Yan, Xiaowei Dong, Qijun Yao, Haidong Liang

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Translational cancer research · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

8 authors at 1 institution in 1 country.

Ziang Zheng *Department of Bone and Soft Tissue Repair and Reconstructive Surgery, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Dalian, 116000, Liaoning, China.
Xinghan Zhao *Department of Bone and Soft Tissue Repair and Reconstructive Surgery, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Dalian, 116000, Liaoning, China.
Bo YuanDepartment of Bone and Soft Tissue Repair and Reconstructive Surgery, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Dalian, 116000, Liaoning, China.
Shan JiangDepartment of Bone and Soft Tissue Repair and Reconstructive Surgery, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Dalian, 116000, Liaoning, China.
Rushan YanDepartment of Bone and Soft Tissue Repair and Reconstructive Surgery, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Dalian, 116000, Liaoning, China.
Xiaowei DongDepartment of Bone and Soft Tissue Repair and Reconstructive Surgery, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Dalian, 116000, Liaoning, China.
Qijun YaoDepartment of Bone and Soft Tissue Repair and Reconstructive Surgery, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Dalian, 116000, Liaoning, China.
Haidong LiangDepartment of Bone and Soft Tissue Repair and Reconstructive Surgery, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Dalian, 116000, Liaoning, China. johnlhddmu@outlook.com.ORCID 0009-0003-0085-2449
Dalian Medical University · CN

Funding

The cultivating scientific research project of the Second Hospital of Dalian Medical University dy2yynpy202219
6 · The paper itself

Abstract

backgroundSoy isoflavones (SI) is a natural bioactive substance exhibiting beneficial effects on human health. This study aims to elucidate the therapeutic potential of SI in the treatment of osteosarcoma (OS) and to investigate the underlying mechanisms, particularly focusing on mitophagy.

methodsThe effects of SI on the proliferation, apoptosis, migration, and invasion of U2OS cells were analyzed. Mitophagy was assessed through multiple parameters: mitochondrial autophagosomes, mitochondrial membrane potential, autophagy-related proteins, reactive oxygen species (ROS), and oxygen consumption rate (OCR). Protein levels related to apoptosis, autophagy, and the AKT/mTOR pathway were analyzed using western blot. The therapeutic efficacy of SI was further identified using a mouse tumor xenograft model. Cell apoptosis and proliferation in tumor xenografts were detected by TUNEL staining and immunohistochemistry (IHC), respectively.

resultsSI dose-dependently suppressed the viability, colony formation, migration, and invasion of U2OS cells, and enhanced the apoptosis. SI also dose-dependently induced mitophagy in OS cells, evidenced by an increase in autophagosomes and ROS levels, a decrease in mitochondrial membrane potential and OCR, and concomitant changes in autophagy-related proteins. Mdivi-1, an inhibitor of mitophagy, reversed the anti-tumor effects of SI on U2OS cells. In addition, SI blocked the AKT/mTOR pathway in U2OS cells. SC-79, an AKT agonist, reversed the effect of SI on inducing mitophagy. Moreover, SI also promoted cell apoptosis and mitophagy in tumor xenografts in vivo.

conclusionsSI induces mitophagy in OS cells by blocking the AKT/mTOR pathway, contributing to the inhibition of OS.

Indexed as

Bone NeoplasmsIsoflavonesOsteosarcomaAnimalsAutophagy-Related ProteinsDisease Models, AnimalGlycine maxHumansMiceMitophagyProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSignal TransductionTOR Serine-Threonine KinasesAutophagy-Related ProteinsIsoflavonesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTOR Serine-Threonine KinasesAKT/mTOR pathwayAutophagyMitophagyOsteosarcomaSoy isoflavones

Identifiers

PMID38191316
PMCPMC10775635
OpenAlexW4390658841

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.