Evidence map›Paper›PMID 31215481›Full record

ArticleBMC cancer2019

MiR-7-5p-mediated downregulation of PARP1 impacts DNA homologous recombination repair and resistance to doxorubicin in small cell lung cancer.

Jinzhi Lai, Hainan Yang, Yanyang Zhu, Mei Ruan, Yayu Huang, Qiuyu Zhang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 2 pooled it
5.4field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 89 citations in OpenAlex.

  1. Pooled it
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  6. Article
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  8. A Robust NSCLC Biomarker- miR-7-5p: ItsMicroRNA (Shariqah, United Arab Emirates) · 2025
    Article
  9. Review
  10. Article
  11. Non-Coding RNAs as Key Regulators in Lung Cancer.International journal of molecular sciences · 2023
    Review
  12. miRNAs as short non-coding RNAs in regulating doxorubicin resistance.Journal of cell communication and signaling · 2023
    Review
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  14. 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

6 authors at 1 institution in 1 country.

Jinzhi LaiDepartment of Oncology, The Second Affiliated Hospital, Fujian Medical University, Quanzhou, China.
Hainan YangDepartment of Ultrasound, The Second Affiliated Hospital, Fujian Medical University, Quanzhou, China.
Yanyang ZhuInstitute of Immunotherapy, Fujian Medical University, Fuzhou, 350108, Fujian, China.
Mei RuanInstitute of Immunotherapy, Fujian Medical University, Fuzhou, 350108, Fujian, China.
Yayu HuangDepartment of Oncology, The Second Affiliated Hospital, Fujian Medical University, Quanzhou, China.
Qiuyu ZhangInstitute of Immunotherapy, Fujian Medical University, Fuzhou, 350108, Fujian, China. qiuyu.zhang@fjmu.edu.cn.ORCID http://orcid.org/0000-0003-4081-7480
Fujian Medical University · CN

Funding

Fujian Provincial Department of Science and Technology 2016-1-69Fujian Provincial Department of Science and Technology WKJ2016-2-31Natural Science Foundation of Fujian Province 2016J01516
6 · The paper itself

Abstract

backgroundChemo-resistance is one of the major challenges in the therapy of small cell lung cancer (SCLC). Multiple mechanisms are thought to be involved in chemo-resistance during SCLC treatment, but unfortunately, these mechanisms have not been well elucidated. Herein, we investigated the role of miRNA in the resistance of SCLC cells to doxorubicin (Dox).

methodsMiRNA microarray analysis revealed that several miRNAs, including miR-7-5p, were specifically decreased in Dox-resistant SCLC cells (H69AR) compared to parental cells (H69). The expression level of miR-7-5p was confirmed by qRT-PCR in Dox-resistant cells (H69AR and H446AR cells) and their parental cells. Bioinformatic analysis indicated that poly ADP-ribose polymerase 1 (PARP1) is a direct target of miR-7-5p. The binding sites of miR-7-5p in the PARP1 3' UTR were verified by luciferase reporter and Western blot assays. To investigate the role of miR-7-5p in the chemo-resistance of SCLC cells to doxorubicin, mimic or inhibitor of miR-7-5p was transfected into SCLC cells, and the effect of miR-7-5p on homologous recombination (HR) repair was analyzed by HR reporter assays. Furthermore, the expression of HR repair factors (Rad51 and BRCA1) induced by doxorubicin was detected by Western blot and immunofluorescent staining in H446AR cells transfected with miR-7-5p mimic.

resultsThe expression level of miR-7-5p was remarkably reduced (4-fold) in Dox-resistant SCLC cells (H69AR and H446AR cells) compared with that in parental cells (H69 and H446 cells). Poly ADP-ribose polymerase 1 (PARP1) is a direct target of miR-7-5p, and PARP1 expression was downregulated by miR-7-5p. MiR-7-5p impeded Dox-induced HR repair by inhibiting the expression of HR repair factors (Rad51 and BRCA1) that resulted in resensitizing SCLC cells to doxorubicin.

conclusionsOur findings provide evidence that miR-7-5p targets PARP1 to exert its suppressive effects on HR repair, indicating that the alteration of the expression of miR-7-5p may be a promising strategy for overcoming chemo-resistance in SCLC therapy.

Indexed as

Antibiotics, AntineoplasticCarrier ProteinsCell Line, TumorDNA RepairDown-RegulationDoxorubicinDrug Resistance, NeoplasmHumansLung NeoplasmsMicroRNAsPoly (ADP-Ribose) Polymerase-1Recombinational DNA RepairSmall Cell Lung CarcinomaUbiquitin-Protein LigasesAntibiotics, AntineoplasticBRAP protein, humanCarrier ProteinsDoxorubicinMicroRNAsMIRN7-1 microRNA, humanPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1RAD51 associated protein 2, humanUbiquitin-Protein LigasesChemo-resistanceDoxorubicinHomologous recombinationMiR-7-5pPoly ADP-ribose polymerase 1Small cell lung cancer

Identifiers

PMID31215481
PMCPMC6582543
OpenAlexW2949603616

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.