Evidence map›Paper›PMID 27002217›Full record

ArticleCell research2016

CCAR1 5' UTR as a natural miRancer of miR-1254 overrides tamoxifen resistance.

Gaopeng Li, Xiaoli Wu, Wenchang Qian, Huayong Cai, Xinbao Sun, Weijie Zhang, Sheng Tan, Zhengsheng Wu, Pengxu Qian, Keshuo Ding and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Cell research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  5. Advancing Ischemic Stroke Prognosis: Key Role of MiR-155 Non-Coding RNA.International journal of molecular sciences · 2025
    Review
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  11. A plant virus manipulates the long-winged morph of insect vectors.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Article
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  19. 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

19 authors at 6 institutions in 3 countries.

Gaopeng LiThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xiaoli WuThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Wenchang QianThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Huayong CaiThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xinbao SunThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Weijie ZhangThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Sheng TanThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Zhengsheng WuDepartment of Pathology, Anhui Medical University, Hefei, Anhui 230027, China.
Pengxu QianStowers Institute for Medical Research, Kansas City, Missouri 64110, USA.
Keshuo DingDepartment of Pathology, Anhui Medical University, Hefei, Anhui 230027, China.
Xuefei LuThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xiao ZhangThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Hong YanDepartment of Pathology, Anhui Medical University, Hefei, Anhui 230027, China.
Haifeng SongDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Shouhong GuangThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Qingfa WuThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Peter E LobieCancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore 117599, Singapore.
Ge ShanThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Tao ZhuThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
University of Science and Technology of China · CNHefei National Center for Physical Sciences at Nanoscale · CNAnhui Medical University · CNBeijing Radiation Center · CNNational University of Singapore · SGStowers Institute for Medical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) typically bind to unstructured miRNA-binding sites in target RNAs, leading to a mutual repression of expression. Here, we report that miR-1254 interacts with structured elements in cell cycle and apoptosis regulator 1 (CCAR1) 5' untranslated region (UTR) and this interaction enhances the stability of both molecules. miR-1254 can also act as a repressor when binding to unstructured sites in its targets. Interestingly, structured miR-1254-targeting sites act as both a functional RNA motif-sensing unit, and an independent RNA functional unit that enhances miR-1254 expression. Artificially designed miRNA enhancers, termed "miRancers", can stabilize and enhance the activity of miRNAs of interest. We further demonstrate that CCAR1 5' UTR as a natural miRancer of endogenous miR-1254 re-sensitizes tamoxifen-resistant breast cancer cells to tamoxifen. Thus, our study presents a novel model of miRNA function, wherein highly structured miRancer-like motif-containing RNA fragments or miRancer molecules specifically interact with miRNAs, leading to reciprocal stabilization.

Indexed as

3' Untranslated Regions5' Untranslated RegionsApoptosis Regulatory ProteinsArgonaute ProteinsBase SequenceBreast NeoplasmsCell Cycle ProteinsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsModels, BiologicalRNA StabilityTamoxifen3' Untranslated Regions5' Untranslated RegionsAGO2 protein, humanApoptosis Regulatory ProteinsArgonaute ProteinsCCAR1 protein, humanCell Cycle ProteinsMicroRNAsMIRN1254 microRNA, humanTamoxifen

Identifiers

PMID27002217
PMCPMC4897177
OpenAlexW2310765949

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.