Evidence map›Paper›PMID 32922184›Full record

ArticleInternational journal of medical sciences2020

NAD(P)H:quinone oxidoreductase 1 determines radiosensitivity of triple negative breast cancer cells and is controlled by long non-coding RNA NEAT1.

Li-Ching Lin, Hsueh-Te Lee, Peng-Ju Chien, Yu-Hao Huang, Mu-Ya Chang, Yueh-Chun Lee, Wen-Wei Chang

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

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  14. Emerging roles of the long non-coding RNA NEAT1 in gynecologic cancers.Journal of cell communication and signaling · 2023
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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

7 authors at 4 institutions in 1 country.

Li-Ching LinDepartment of Radiation Oncology, Chi-Mei Foundation Medical Center, Tainan, Taiwan.
Hsueh-Te LeeInstitute of Anatomy and Cell Biology, School of Medicine, National Yang Ming University, Taipei City, Taiwan.
Peng-Ju ChienSchool of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Yu-Hao HuangSchool of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Mu-Ya ChangSchool of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Yueh-Chun LeeDepartment of Radiation Oncology, Chung Shan Medical University Hospital, Taichung, Taiwan.
Wen-Wei ChangSchool of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWChung Shan Medical University Hospital · TWChi Mei Medical Center · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radioresistant cells cause recurrence in patients with breast cancer after they undergo radiation therapy. The molecular mechanisms by which cancer cells obtain radioresistance should be understood to develop radiation-sensitizing agents. Results showed that the protein expression and activity of NAD(P)H:quinone oxidoreductase 1 (NQO1) were upregulated in radioresistant MDA-MB-231 triple-negative breast cancer (TNBC) cells. NQO1 knockdown inhibited the proliferation of NQO1 expressing Hs578t TNBC cells or the radioresistant MDA-MB-231 cells, whereas NOQ1 overexpression increased the survival of MDA-MB-231 cells, which lack of NQO1 expression originally, under irradiation. The cytotoxicity of β-lapachone, an NQO1-dependent bioactivatable compound, was greater in radioresistant MDA-MB-231 cells than in parental cells. β-lapachone displayed a radiosensitization effect on Hs578t or radioresistant MBDA-MB-231 cells. The expression of the long noncoding RNA NEAT1 positively regulated the NQO1 expression in radioresistant MDA-MB-231 cells at a translational level rather than at a transcription level. The inhibition of the NEAT1 expression through the CRISPR-Cas9 method increased the sensitivity of radioresistant MDA-MB-231 cells to radiation and decreased their proliferation, the activity of cancer stem cells, and the expression of stemness genes, including BMI1, Oct4, and Sox2. In conclusion, the NQO1 expression in triple-negative breast cancer cells determined their radiosensitivity and was controlled by NEAT1. In addition, NOQ1 bioactivatable compounds displayed potential for application in the development of radiation sensitizers in breast cancer.

Indexed as

Cell Line, TumorCell ProliferationCell SurvivalFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansNAD(P)H Dehydrogenase (Quinone)NaphthoquinonesNeoplastic Stem CellsRadiation-Sensitizing AgentsRadiation ToleranceRNA, Long NoncodingTriple Negative Breast Neoplasmsbeta-lapachoneNAD(P)H Dehydrogenase (Quinone)NaphthoquinonesNEAT1 long non-coding RNA, humanNQO1 protein, humanRadiation-Sensitizing AgentsRNA, Long Noncodinglong non-coding RNA NEAT1NAD(P)H:quinone oxidoreductase 1radiosensitivitytriple negative breast cancer

Identifiers

PMID32922184
PMCPMC7484675
OpenAlexW3084205269

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.