Evidence map›Paper›PMID 25348507›Full record

ArticleCell proliferation2014

miR-99a directly targets the mTOR signalling pathway in breast cancer side population cells.

Z Yang, Y Han, K Cheng, G Zhang, X Wang

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.4field-weighted citation impact, top 7% 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, 93 citations in OpenAlex.

  1. Article
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  11. MicroRNA Regulation of Breast Cancer Stemness.International journal of molecular sciences · 2021
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  12. Review
  13. The Emerging Roles of Autophagy-Related MicroRNAs in Cancer.International journal of biological sciences · 2021
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  14. Review
  15. Article
  16. The interplay between HIF-1α and noncoding RNAs in cancer.Journal of experimental & clinical cancer research : CR · 2020
    Review
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Z YangDepartment of Breast and Thyroid Surgery, Affiliated Hospital of Binzhou Medical University, Binzhou, Shandong, 256603, China.
Y Han
K Cheng
G Zhang
X Wang
Binzhou Medical University · CNBinzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesmiR-99a has been reported to function as a tumour suppressor in breast cancer. However, its role in the regulation of breast cancer stem cell (CSC) phenotype has up to now remained unknown. MATERIALS AND

methodsIn this study, we isolated the side population (SP) cells by staining cultured MCF-7 and MDA-MB-231 cells with fluorescent DNA-binding dye Hoechst 33342, then by flow cytometric sorting. Next, we detected expression of miR-99a in the SP cells compared to non-SP cells using real-time PCR, and explored effects of miR-99a on the CSC phenotype of the breast cancer cells, including sphere formation, self-renewal, tumourigenicity and cell migratory capability.

resultsWe found that expression of miR-99a was down-regulated in the SP cells compared to non-SP cells. Restoration of expression of miR-99a inhibited cell migration and invasion, reduced sphere formation of breast SP cells in vitro, and suppressed tumour growth in vivo. Finally, bioinformatic prediction suggested the oncogene, mammalian target of rapamycin (mTOR) - a downstream effector of the PI3K/AKT signalling pathway, was a target gene of miR-99a in SP cells. Further, quantitative RT-PCR and western blot assays identified that overexpression of miR-99a suppressed expression of mTOR and its downstream gene, HIF-1α.

conclusionCollectively, these data suggest that miR-99a reversed the breast cancer malignant CSC phenotype, probably by targeting the mTOR signalling pathway.

Indexed as

Signal TransductionAnimalsBase SequenceBreast NeoplasmsCell Line, TumorCell MovementFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMCF-7 CellsMiceMice, Inbred BALB CMice, NudeMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN99 microRNA, humanMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID25348507
PMCPMC6495876
OpenAlexW2110257299

What OpenQuestion holds

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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.