Evidence map›Paper›PMID 26918449›Full record

ArticleOncotarget2016

miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation.

Tongbao Feng, Fang Shao, Qiyong Wu, Xiaohang Zhang, Dongqin Xu, Keqing Qian, Yewen Xie, Shizhong Wang, Ning Xu, Yong Wang and 1 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
  2. Review
  3. Longitudinal tracking ofMolecular therapy. Oncology · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. Downregulation ofBiochemistry and biophysics reports · 2024
    Article
  8. Review
  9. Review
  10. Review
  11. Interplay between LncRNAs and microRNAs in Breast Cancer.International journal of molecular sciences · 2023
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

12 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 2 countries.

Tongbao FengMedical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Fang ShaoMedical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Qiyong WuDepartment of General Surgery, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Xiaohang ZhangMedical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Dongqin XuMedical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Keqing QianMedical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Yewen XieMedical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Shizhong WangMedical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Ning XuSection of Clinical Chemistry and Pharmacology, Department of Laboratory Medicine, Lund University, S-221 85 Lund, Sweden.
Yong WangDepartment of General Surgery, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Chunjian QiMedical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
Nanjing Medical University · CNChangzhou No.2 People's Hospital · CNLund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been recently shown to be dysregulated in several cancers. However, the mechanisms underlying the role of MALAT1 in breast cancer remain unclear. Herein, we showed that MALAT1 was aberrantly increased in breast cancer tissues and cells. MALAT1-siRNA inhibited breast cancer cell proliferation and cell cycle progression in vitro and in vivo. Furthermore, MALAT1 acted as an endogenous potent regulator by directly binding to miR-124 and down-regulating miR-124 expression. In addition, MALAT1 reversed the inhibitory effect of miR-124 on breast cancer proliferation and was involved in the cyclin-dependent kinase 4 (CDK4) expression. Taken together, our data highlight the pivotal role of MALAT1 in breast cancer tumorigenesis. Moreover, the present study elucidated the MALAT1-miR-124-CDK4/E2F1 signaling pathway in breast cancer, which might provide a new approach for tackling breast cancer.

Indexed as

AnimalsBreast NeoplasmsCyclin-Dependent Kinase 4Disease ProgressionDown-RegulationE2F1 Transcription FactorFemaleGene Expression Regulation, NeoplasticHeterograftsHumansKaplan-Meier EstimateMiceMice, NudeMicroRNAsRNA, Long NoncodingCDK4 protein, humanCyclin-Dependent Kinase 4E2F1 protein, humanE2F1 Transcription FactorMALAT1 long non-coding RNA, humanMicroRNAsMIRN124 microRNA, humanRNA, Long Noncodingbreast cancercell cyclecyclin-dependent kinase 4MALAT1miR-124

Identifiers

PMID26918449
PMCPMC4941308
OpenAlexW2291490667

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.