Evidence map›Paper›PMID 25611379›Full record

ArticleCell death & disease2015

Celastrol induces apoptosis and autophagy via the ROS/JNK signaling pathway in human osteosarcoma cells: an in vitro and in vivo study.

H-Y Li, J Zhang, L-L Sun, B-H Li, H-L Gao, T Xie, N Zhang, Z-M Ye

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

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 1 pooled it
69.2field-weighted citation impact, top 1% 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

145 citing papers in PubMed, 1 synthesis or guideline pooled it, 280 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. A new perspective on iron-dependent cell death: PRDX-1-mediated ferroptosis in tumor cells.Apoptosis : an international journal on programmed cell death · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

85 more citing papers are in PubMed but not listed here.

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.

H-Y LiDepartment of Orthopedics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
J ZhangDepartment of Orthopedics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
L-L SunDepartment of Orthopedics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
B-H LiDepartment of Orthopedics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
H-L GaoDepartment of Orthopedics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
T XieDepartment of Orthopedics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
N ZhangDepartment of Orthopedics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Z-M YeDepartment of Orthopedics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma is the most common primary malignant tumor of bone, the long-term survival of which has stagnated in the past several decades. Celastrol, a triterpene from traditional Chinese medicine, has been proved to possess potent anti-tumor effect on various cancers. However, the effect of celastrol on human osteosarcoma and the underlying mechanisms remains to be elucidated. We reported here that celastrol could inhibit cell proliferation by causing G2/M phase arrest. Exposure to celastrol resulted in the activation of caspase-3, -8, and -9, indicating that celastrol induced apoptosis through both extrinsic and intrinsic pathways. Autophagy occurred in celastrol-treated cells as evidenced by formation of autophagosome and accumulation of LC3B-II. The celastrol-induced cell death was remarkably restored by the combination of autophagy and apoptosis inhibitors. Furthermore, inhibition of apoptosis enhanced autophagy while suppression of autophagy diminished apoptosis. Celastrol also induced JNK activation and ROS generation. The JNK inhibitor significantly attenuated celastrol-triggered apoptosis and autophagy while ROS scavenger could completely reverse them. The ROS scavenger also prevented G2/M phase arrest and phosphorylation of JNK. Importantly, we found that celastrol had the similar effects on primary osteosarcoma cells. Finally, in vivo, celastrol suppressed tumor growth in the mouse xenograft model. Taken together, our results revealed that celastrol caused G2/M phase arrest, induced apoptosis and autophagy via the ROS/JNK signaling pathway in human osteosarcoma cells. Celastrol is therefore a promising candidate for development of antitumor drugs targeting osteosarcoma.

Indexed as

AnimalsApoptosisAutophagyCaspasesCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCell ProliferationEnzyme ActivationFemaleFibroblastsHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMice, Inbred BALB CMice, NudeCaspasescelastrolCell Cycle ProteinsJNK Mitogen-Activated Protein KinasesPentacyclic TriterpenesReactive Oxygen SpeciesTriterpenes

Identifiers

PMID25611379
PMCPMC4669742
OpenAlexW2119316865

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.