Evidence map›Paper›PMID 27323416›Full record

ArticleOncotarget2016

Androgen-induced miR-135a acts as a tumor suppressor through downregulating RBAK and MMP11, and mediates resistance to androgen deprivation therapy.

Xuechao Wan, Honglei Pu, Wenhua Huang, Shu Yang, Yalong Zhang, Zhe Kong, Zhuoran Yang, Peiqing Zhao, Ao Li, Tao Li and 1 more

Abstract read
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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Modulation of Immune Response toFrontiers in cellular and infection microbiology · 2021
    Article
  11. Review
  12. Article
  13. Review
  14. Androgen-Regulated microRNAs (AndroMiRs) as Novel Players in Adipogenesis.International journal of molecular sciences · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. miR-192 Is Overexpressed and Promotes Cell Proliferation in Prostate Cancer.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2019
    Article
  19. Review
  20. Circular RNA Myosin Light Chain Kinase (MYLK) Promotes Prostate Cancer Progression through Modulating Mir-29a Expression.Medical science monitor : international medical journal of experimental and clinical research · 2018
    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

11 authors.

Xuechao WanState Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Science, Fudan University, Shanghai, 200433, PR China.
Honglei PuState Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Science, Fudan University, Shanghai, 200433, PR China.
Wenhua HuangState Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Science, Fudan University, Shanghai, 200433, PR China.
Shu YangState Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Science, Fudan University, Shanghai, 200433, PR China.
Yalong ZhangState Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Science, Fudan University, Shanghai, 200433, PR China.
Zhe KongState Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Science, Fudan University, Shanghai, 200433, PR China.
Zhuoran YangState Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Science, Fudan University, Shanghai, 200433, PR China.
Peiqing ZhaoCenter of Translational Medicine, Central Hospital of Zibo, Zibo, Shangdong, 255036, PR China.
Ao LiCenter of Translational Medicine, Central Hospital of Zibo, Zibo, Shangdong, 255036, PR China.
Tao LiCenter of Translational Medicine, Central Hospital of Zibo, Zibo, Shangdong, 255036, PR China.
Yao LiState Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Science, Fudan University, Shanghai, 200433, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main challenge in the treatment of prostate cancer (PCa) is that the majority of patients inevitably develop resistance to androgen deprivation. However, the mechanisms involved in hormone independent behavior of PCa remain unclear. In the present study, we identified androgen-induced miR-135a as a direct target of AR. Functional studies revealed that overexpression of miR-135a could significantly decrease cell proliferation and migration, and induce cell cycle arrest and apoptosis in PCa. We identified RBAK and MMP11 as direct targets of miR-135a in PCa by integrating bioinformatics analysis and experimental assays. Mechanistically, miR-135a repressed PCa migration through downregulating MMP11 and induced PCa cell cycle arrest and apoptosis by suppressing RBAK. Consistently, inverse correlations were also observed between the expression of miR-135a and RBAK or MMP11 in PCa samples. In addition, low miR-135a and high RBAK and MMP11 expression were positively correlated with PCa progression. Also, PI3K/AKT pathway was confirmed to be an upstream regulation signaling of miR-135a in androgen-independent cell lines. Accordingly, we reported a resistance mechanism to androgen deprivation therapy (ADT) mediated by miR-135a which might be downregulated by androgen depletion and/or PI3K/AKT hyperactivation, in castration-resistant prostate cancer (CRPC), thus promoting tumor progression. Taken together, miR-135a may represent a new diagnostic and therapeutic biomarker for castration-resistant PCa.

Indexed as

Androgen AntagonistsAndrogensAntineoplastic Agents, HormonalCell Line, TumorCell ProliferationDown-RegulationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansMaleMatrix Metalloproteinase 11MicroRNAsProstatic Neoplasms, Castration-ResistantRepressor ProteinsAndrogen AntagonistsAndrogensAntineoplastic Agents, HormonalMatrix Metalloproteinase 11MicroRNAsMIRN135 microRNA, humanMMP11 protein, humanRBaK protein, humanRepressor Proteinsandrogen receptormiR-135aMMP11PI3K/AKTRBAK

Identifiers

PMID27323416
PMCPMC5239475

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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.