Evidence map›Paper›PMID 37227155›Full record

ArticleActa biochimica et biophysica Sinica2023

The FBXO32/ATR/ATM axis acts as a molecular switch to control the sensitivity of osteosarcoma cells to irradiation through its regulation of EXO1 expression.

Yao Lu, Panpan Huang, Yanli Li, Wenyu Liu, Jing Li, Rui Zhao, Haihua Feng, Ce Shi, Gaolu Cao

Open access · diamondAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

Yao LuSchool of Basic Medicine, Gannan Medical University, Ganzhou 341000, China.
Panpan HuangSchool of Basic Medicine, Gannan Medical University, Ganzhou 341000, China.
Yanli LiDepartment of Pharmacy, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Wenyu LiuSchool of Basic Medicine, Gannan Medical University, Ganzhou 341000, China.
Jing LiSchool of Basic Medicine, Gannan Medical University, Ganzhou 341000, China.
Rui ZhaoSchool of Basic Medicine, Gannan Medical University, Ganzhou 341000, China.
Haihua FengDepartment of Radiation Oncology, City of Hope National Medical Center, Duarte, CA 91010, USA.
Ce ShiDepartment of Orthopedics, the Affiliated Suqian Hospital of Xuzhou Medical University, Suqian 223800, China.
Gaolu CaoSchool of Basic Medicine, Gannan Medical University, Ganzhou 341000, China.
Gannan Medical University · CNCity Of Hope National Medical Center · USThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma (OS) is the most common primary bone cancer in children and adolescents. In clinical treatments, the insensitivity of OS to conventional radiotherapy regimens significantly contributes to poor patient prognosis and survival. EXO1 is responsible for DNA repair pathways and telomere maintenance. Meanwhile, ATM and ATR are considered switches because they can regulate the expression of EXO1. However, their expression and interaction in OS cells under irradiation (IR) remain unclear. This study aims to investigate the roles of FBXO32, ATM, ATR and EXO1 in OS radiotherapy insensitivity and poor patient prognosis and explore potential pathogenic mechanisms. Bioinformatics is employed to analyse differential gene expression and correlations with prognosis in OS. Cell counting kit 8 assay, clone formation assay, and flow cytometry are used to evaluate cell survival and apopotosis under IR. Co-IP assay is used to detect protein‒protein interactions. Bioinformatics analysis reveals that EXO1 is closely related to survival, apoptosis and poor prognosis in OS. Silencing of

Indexed as

Bone NeoplasmsOsteosarcomaAdolescentAtaxia Telangiectasia Mutated ProteinsCell Line, TumorCell ProliferationCell SurvivalChildDNA Repair EnzymesExodeoxyribonucleasesHumansMuscle ProteinsSKP Cullin F-Box Protein LigasesAtaxia Telangiectasia Mutated ProteinsATM protein, humanATR protein, humanDNA Repair EnzymesEXO1 protein, humanExodeoxyribonucleasesFBXO32 protein, humanMuscle ProteinsSKP Cullin F-Box Protein LigasesATMATREXO1FBXO32irradiationosteosarcoma

Identifiers

PMID37227155
PMCPMC10281878
OpenAlexW4327751118

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.