Evidence map›Paper›PMID 29393495›Full record

ArticleOncology reports2018

miR-195 inhibits cell proliferation and angiogenesis in human prostate cancer by downregulating PRR11 expression.

Chao Cai, Huichan He, Xiaolu Duan, Wenqi Wu, Zanlin Mai, Tao Zhang, Junhong Fan, Tuo Deng, Wen Zhong, Yongda Liu and 2 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Oncology reports, 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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Chao CaiDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Huichan HeDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Xiaolu DuanDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Wenqi WuDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Zanlin MaiDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Tao ZhangDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Junhong FanDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Tuo DengDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Wen ZhongDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Yongda LiuDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Weide ZhongDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Guohua ZengDepartment of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University and Guangdong Key Laboratory of Urology, Guangzhou, Guangdong 510230, P.R. China.
Guangzhou Medical University · CNFirst Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

hsa-miR-195-5p (miR-195) has been proven to be a critical regulator in the progression of prostate cancer (PCa). To identify additional targets and molecular functions of miR-195, we overexpressed miR-195 by transient oligonucleotide transfection in DU145 and LNCaP cells and examined the effects. RNA-based microarray and dual-luciferase assays were carried out to identify novel targets of miR-195, while in vitro functional assays, a subcutaneous xenograft model, tissue microarray (TMA) analysis and a cohort of publicly available data (Taylor cohort) were used to investigate the biological function and clinical value of miR-195 targeting. The results shown that miR-195 overexpression could markedly suppress cellular proliferation and tube formation compared with miR-negative control. The RNA-based microarray identified a total of 153 differentially regulated genes with fold changes of ≤|1.5|, including 138 (90.2%) downregulated and 15 (9.8%) upregulated genes. Among the downregulated genes, we found that proline-rich protein 11 (PRR11) combined with miR-195 expression (miR-195/PRR11) could be used as an independent predictor of the risk of biochemical recurrence in the Taylor cohort. Additionally, the dual-luciferase assay identified PRR11 as a novel target of miR-195, and the in vitro assays indicated that PRR11 abrogated the suppressive effects of miR-195 on cell proliferation, tube formation and cell cycling. Furthermore, the subcutaneous tumor xenograft model indicated that knockdown of PRR11 inhibited xenograft growth and angiogenesis, while the results of the TMA and Taylor cohort analyses collectively demonstrated that PRR11 expression was upregulated in aggressive tumors and is associated with poor clinical outcome. Taken together, these findings further illustrate the suppressive role of miR-195 in PCa, and indicate a novel role of PRR11 in PCa. Importantly, the newly identified miR-195/PRR11 axis may aid with identifying potential therapeutic targets in PCa.

Indexed as

AnimalsApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMaleMiceMicroRNAsNeovascularization, PathologicProstatic NeoplasmsProteinsProteomicsXenograft Model Antitumor AssaysMicroRNAsMIRN195 microRNA, humanProteinsPRR11 protein, human

Identifiers

PMID29393495
PMCPMC5868402
OpenAlexW2793686062

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.