Evidence map›Paper›PMID 38645664›Full record

ArticleMedComm2024

Mechanism of Musashi2 affecting radiosensitivity of lung cancer by modulating DNA damage repair.

Hongjin Qu, Xiong Shi, Ying Xu, Hongran Qin, Junshi Li, Shanlin Cai, Jianpeng Zhao, Bingbing Wan, Yanyong Yang, Bailong Li

Open access · goldAbstract read
In one paragraph

Article in MedComm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
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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

10 authors at 4 institutions in 1 country.

Hongjin QuDepartment of Radiation Medicine Faculty of Naval Medicine Naval Medical University Shanghai China.
Xiong ShiShanghai Engineering Research Center of Tooth Restoration and Regeneration Tongji Research Institute of Stomatology Department of Radiology, Stomatological Hospital and Dental School, Tongji University Shanghai China.
Ying XuDepartment of Radiation Medicine Faculty of Naval Medicine Naval Medical University Shanghai China.
Hongran QinDepartment of Nuclear Radiation Shanghai Pulmonary Hospital School of Medicine Tongji University Shanghai China.
Junshi LiDepartment of Radiation Medicine Faculty of Naval Medicine Naval Medical University Shanghai China.
Shanlin CaiDepartment of Radiation Medicine Faculty of Naval Medicine Naval Medical University Shanghai China.
Jianpeng ZhaoDepartment of Radiation Medicine Faculty of Naval Medicine Naval Medical University Shanghai China.
Bingbing WanKey Laboratory of Systems Biomedicine (Ministry of Education) Shanghai Center for Systems Biomedicine Shanghai Jiao Tong University Shanghai China.
Yanyong YangDepartment of Radiation Medicine Faculty of Naval Medicine Naval Medical University Shanghai China.
Bailong LiDepartment of Radiation Medicine Faculty of Naval Medicine Naval Medical University Shanghai China.
Naval University of Engineering · CNShanghai Jiao Tong University · CNShanghai Pulmonary Hospital · CNShanghai Stomatological Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Identifying new targets for overcoming radioresistance is crucial for improving the efficacy of lung cancer radiotherapy, given that tumor cell resistance is a leading cause of treatment failure. Recent research has spotlighted the significance of Musashi2 (MSI2) in cancer biology. In this study, we first demonstrated that MSI2 plays a key function in regulating the radiosensitivity of lung cancer. The expression of MSI2 is negatively correlated with overall survival in cancer patients, and the knockdown of MSI2 inhibits tumorigenesis and increases radiosensitivity of lung cancer cells. Cellular radiosensitivity, which is closely linked to DNA damage, is influenced by MSI2 interaction with ataxia telangiectasia mutated and Rad3-related kinase (ATR) and checkpoint kinase 1 (CHK1) post-irradiation; moreover, knockdown of MSI2 inhibits the ATR-mediated DNA damage response pathway. RNA-binding motif protein 17 (RBM17), which is implicated in DNA damage repair, exhibits increased interaction with MSI2 post-irradiation. We found that knockdown of RBM17 disrupted the interaction between MSI2 and ATR post-irradiation and increased the radiosensitivity of lung cancer cells. Furthermore, we revealed the potential mechanism of MSI2 recruitment into the nucleus with the assistance of RBM17 to activate ATR to promote radioresistance. This study provides novel insights into the potential application of MSI2 as a new target in lung cancer radiotherapy.

Indexed as

ataxia telangiectasia mutated and Rad3‐related kinase (ATR)DNA damage repairlung cancerMusashi2 (MSI2)radioresistanceradiosensitivityRNA‐binding motif protein 17 (RBM17)

Identifiers

PMID38645664
PMCPMC11032739
OpenAlexW4394985636

What OpenQuestion holds

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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.