Evidence map›Paper›PMID 29796115›Full record

ArticleClinical epigenetics2018

miR-29c plays a suppressive role in breast cancer by targeting the TIMP3/STAT1/FOXO1 pathway.

Wan Li, Jie Yi, Xiangjin Zheng, Shiwei Liu, Weiqi Fu, Liwen Ren, Li Li, Dave S B Hoon, Jinhua Wang, Guanhua Du

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  9. Article
  10. The Mechanism of DNA Methylation and miRNA in Breast Cancer.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. STAT3 regulates SRGN and promotes metastasis of nasopharyngeal carcinoma through the FoxO1-miR-148a-5p-CREB1 axis.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. DNMT3A and DNMT3B in Breast Tumorigenesis and Potential Therapy.Frontiers in cell and developmental biology · 2022
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Wan Li *1The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Jie Yi *3Department of Clinical Laboratory, Peking Union Medical College Hospital, Beijing, 100730 China.
Xiangjin Zheng1The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Shiwei Liu4Department of Endocrinology, Shanxi DAYI Hospital, Shanxi Medical University, Taiyuan, 030002 Shanxi China.
Weiqi Fu1The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Liwen Ren1The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Li Li2Key Laboratory of Drug Target Research and Drug Screen, Institute of Materia Medica, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100050 China.
Dave S B Hoon5Department of Translational Molecular Medicine, John Wayne Cancer Institute (JWCI) at Providence Saint John's Health Center, Santa Monica, CA 90404 USA.
Jinhua Wang1The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Guanhua Du1The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking Union Medical College Hospital · CNSaint John's Health Center · USShanxi Dayi Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: miR-29c has been associated with the progression of many cancers. However, the function and mechanism of miR-29c have not been well investigated in breast cancers. Methods: Real-time quantitative PCR was used to assess expression of miR-29c and DNMT3B mRNA. Western blot and immunochemistry were used to examine the expression of DNA methyltransferase 3B (DNMT3B) protein in breast cancer cells and tissues. The functional roles of miR-29c in breast cancer cells such as proliferation, migration, invasion, colony formation, and 3D growth were evaluated using MTT, transwell chambers, soft agar, and 3D Matrigel culture, respectively. In addition, the luciferase reporter assay was used to check if miR-29c binds the 3'UTR of DNMT3B. The effects of miR-29c on the DNMT3B/TIMP3/STAT1/FOXO1 pathway were also examined using Western blot and methyl-specific qPCR. The specific inhibitor of STAT1, fludarabine, was used to further check the mechanism of miR-29c function in breast cancer cells. Studies on cell functions were carried out in DNMT3B siRNA cell lines. Results: The expression of miR-29c was decreased with the progression of breast cancers and was closely associated with an overall survival rate of patients. Overexpression of miR-29c inhibited the proliferation, migration, invasion, colony formation, and growth in 3D Matrigel while knockdown of miR-29c promoted these processes in breast cancer cells. In addition, miR-29c was found to bind 3'UTR of DNMT3B and inhibits the expression of DNMT3B, which was elevated in breast cancers. Moreover, the protein level of TIMP3 was reduced whereas methylation of TIMP3 was increased in miR-29c knockdown cells compared to control. On the contrary, the protein level of TIMP3 was increased whereas methylation of TIMP3 was reduced in miR-29c-overexpressing cells compared to control. Knockdown of DNMT3B reduced the proliferation, migration, and invasion of breast cancer cell lines. Finally, our results showed that miR-29c exerted its function in breast cancers by regulating the TIMP3/STAT1/FOXO1 pathway. Conclusion: The results suggest that miR-29c plays a significant role in suppressing the progression of breast cancers and that miR-29c may be used as a biomarker of breast cancers.

Indexed as

Down-RegulationSignal Transduction3' Untranslated RegionsBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3BFemaleForkhead Box Protein O1Gene Expression Regulation, NeoplasticHumansMCF-7 CellsMicroRNAs3' Untranslated RegionsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BForkhead Box Protein O1FOXO1 protein, humanMicroRNAsMIRN29a microRNA, humanSTAT1 protein, humanSTAT1 Transcription FactorTIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3Breast cancerDNMT3B, methylation, and STAT1/FOXO1miR-29c

Identifiers

PMID29796115
PMCPMC5956756
OpenAlexW2805388105

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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.