Evidence map›Paper›PMID 33125136›Full record

ArticleOncology reports2020

Radiosensitizing effects of c‑myc gene knockdown‑induced G2/M phase arrest by intrinsic stimuli via the mitochondrial signaling pathway.

Yunpeng Fan, Xiaofeng Jia, Tao Xie, Liulong Zhu, Fan He

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Intronic polyadenylation-derived long noncoding RNA modulates nucleolar integrity and function.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
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  9. Review
  10. The roles of glycolysis in osteosarcoma.Frontiers in pharmacology · 2022
    Review
  11. Article
  12. Article
  13. Radiation Response of Human Leukemia/Lymphoma Cells was Improved by 7-Geranyloxycoumarin.Dose-response : a publication of International Hormesis Society
    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

5 authors at 4 institutions in 1 country.

Yunpeng FanThe Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Xiaofeng JiaCollege of Life Science, China Jiliang University, Hangzhou, Zhejiang 310018, P.R. China.
Tao XieAffiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310006, P.R. China.
Liulong ZhuThe Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Fan HeAffiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310006, P.R. China.
Hangzhou Medical College · CNChina Jiliang University · CNHangzhou First People's Hospital · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma is the most common primary malignant bone tumor in children and adolescents and its long‑term survival rate has stagnated in the past decades. Previous studies have shown that tumors in the G2/M phase are more sensitive to radiotherapy. The proto‑oncogene c‑myc is a transformed member of the myc family and c‑myc‑interacting zinc finger protein‑1 (Miz‑1) is a poly‑Cys2His2 zinc finger (ZF) activator of cell cycle regulator genes, such as the cyclin‑dependent kinase inhibitor p21. C‑myc can repress the expression of p21 by binding to Miz‑1 and abolishing the interaction between Miz‑1 and its co‑activators, which induces G2/M phase arrest. Therefore, the present study investigated the radiosensitizing effects of the c‑myc gene and the sensitizing apoptosis pathway, aiming to identify a more effective combination radiotherapy treatment for osteosarcoma. The present study demonstrated that the c‑myc gene was overexpressed in osteosarcoma cells compared to osteoblasts. Following inhibition of c‑myc gene expression in osteosarcoma cells, tumor proliferation was significantly hindered after inducing G2/M phase arrest via regulating G2/M phase‑associated proteins. Additionally, it was revealed that inhibiting c‑myc gene expression combined with radiotherapy could significantly increase the apoptosis rate of osteosarcoma cells via the mitochondrial signaling pathway. In summary, the present study verified the radiosensitizing effects of c‑myc gene knockdown‑induced G2/M phase arrest, which was achieved by intrinsic stimuli through the mitochondrial signaling pathway.

Indexed as

ApoptosisBone NeoplasmsCell Line, TumorCell ProliferationDatasets as TopicG2 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansKaplan-Meier EstimateMitochondriaOsteosarcomaProto-Oncogene Proteins c-mycRadiation ToleranceSignal TransductionUp-RegulationMYC protein, humanProto-Oncogene Proteins c-mycc-mycG2/M phase arrestmitochondrialosteosarcomaradiosensitizing

Identifiers

PMID33125136
PMCPMC7640369
OpenAlexW3092783441

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.