Evidence map›Paper›PMID 34611140›Full record

ArticleCell death & disease2021

Aberrantly reduced expression of miR-342-5p contributes to CCND1-associated chronic myeloid leukemia progression and imatinib resistance.

Yi-Ying Wu, Hsing-Fan Lai, Tzu-Chuan Huang, Yu-Guang Chen, Ren-Hua Ye, Ping-Ying Chang, Shiue-Wei Lai, Yeu-Chin Chen, Cho-Hao Lee, Wei-Nung Liu and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  15. Article
  16. Non-Coding RNAs Are Implicit in Chronic Myeloid Leukemia Therapy Resistance.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Frontiers in oncology · 2022
    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

14 authors at 2 institutions in 1 country.

Yi-Ying WuDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Hsing-Fan LaiDepartment of Biochemistry, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Tzu-Chuan HuangDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Yu-Guang ChenDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Ren-Hua YeDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Ping-Ying ChangDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Shiue-Wei LaiDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Yeu-Chin ChenDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Cho-Hao LeeDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Wei-Nung LiuDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Ming-Shen DaiDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Jia-Hong ChenDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Ching-Liang HoDivision of Hematology and Oncology Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, 11490, Taipei, Taiwan, ROC.
Yi-Lin ChiuDepartment of Biochemistry, National Defense Medical Center, 11490, Taipei, Taiwan, ROC. yilin1107@mail.ndmctsgh.edu.tw.ORCID 0000-0002-1827-6924
Tri-Service General Hospital · TWNational Defense Medical Center · TW

Funding

Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) MOST108-2635-B-016-001Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) MOST109-2320-B-016-004Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) MOST-110-2314-B-016-056
6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a myeloproliferative disorder associated with the Philadelphia chromosome, and the current standard of care is the use of tyrosine kinase inhibitors (TKI). However, some patients will not achieve a molecular response and may progress to blast crisis, and the underlying mechanisms remain to be clarified. In this study, next-generation sequencing was used to explore endogenous miRNAs in CML patients versus healthy volunteers, and miR-342-5p was identified as the primary target. We found that miR-342-5p was downregulated in CML patients and had a significant inhibitory effect on cell proliferation in CML. Through a luciferase reporter system, miR-342-5p was reported to target the 3'-UTR domain of CCND1 and downregulated its expression. Furthermore, overexpression of miR-342-5p enhanced imatinib-induced DNA double-strand breaks and apoptosis. Finally, by analyzing clinical databases, we further confirmed that miR-342-5p was associated with predicted molecular responses in CML patients. In conclusion, we found that both in vivo and in vitro experiments and database cohorts showed that miR-342-5p plays a key role in CML patients, indicating that miR-342-5p may be a potential target for future CML treatment or prognostic evaluation.

Indexed as

Disease ProgressionGene Expression Regulation, Leukemic3' Untranslated RegionsAnimalsApoptosisBase SequenceCell Line, TumorCell ProliferationCell SurvivalCyclin D1Disease Models, AnimalDNA Breaks, Double-StrandedDown-RegulationDrug Resistance, NeoplasmGene OntologyHumans3' Untranslated RegionsCCND1 protein, humanCyclin D1Imatinib MesylateMicroRNAsMIRN342 microRNA, humanRNA, Messenger

Identifiers

PMID34611140
PMCPMC8492784
OpenAlexW3202084426

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.