Evidence map›Paper›PMID 22797075›Full record

ArticleOncogene2013

CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer.

C Xie, X H Jiang, J T Zhang, T T Sun, J D Dong, A J Sanders, R Y Diao, Y Wang, K L Fok, L L Tsang and 13 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
7.6field-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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Managing an ageing cystic fibrosis population: challenges and priorities.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  6. The ageing of people living with cystic fibrosis: what to expect now?European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. CFTR and Gastrointestinal Cancers: An Update.Journal of personalized medicine · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Cystic Fibrosis, CFTR, and Colorectal Cancer.International journal of molecular sciences · 2020
    Review

4 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

23 authors at 3 institutions in 2 countries.

C XieEpithelial Cell Biology Research Center, School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, Hong Kong.
X H Jiang
J T Zhang
T T Sun
J D Dong
A J Sanders
R Y Diao
Y Wang
K L Fok
L L Tsang
M K Yu
X H Zhang
Y W Chung
L Ye
M Y Zhao
J H Guo
Z J Xiao
H Y Lan
C F Ng
K M Lau
Z M Cai
W G Jiang
H C Chan
Chinese University of Hong Kong · CNCardiff University · GBPeking University Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis (CF) transmembrane conductance regulator (CFTR) is expressed in the epithelial cells of a wide range of organs/tissues from which most cancers are derived. Although accumulating reports have indicated the association of cancer incidence with genetic variations in CFTR gene, the exact role of CFTR in cancer development and the possible underlying mechanism have not been elucidated. Here, we report that CFTR expression is significantly decreased in both prostate cancer cell lines and human prostate cancer tissue samples. Overexpression of CFTR in prostate cancer cell lines suppresses tumor progression (cell growth, adhesion and migration), whereas knockdown of CFTR leads to enhanced malignancies both in vitro and in vivo. In addition, we demonstrate that CFTR knockdown-enhanced cell proliferation, cell invasion and migration are significantly reversed by antibodies against either urokinase plasminogen activator (uPA) or uPA receptor (uPAR), which are known to be involved in various malignant traits of cancer development. More interestingly, overexpression of CFTR suppresses uPA by upregulating the recently described tumor suppressor microRNA-193b (miR-193b), and overexpression of pre-miR-193b significantly reverses CFTR knockdown-enhanced malignant phenotype and abrogates elevated uPA activity in prostate cancer cell line. Finally, we show that CFTR gene transfer results in significant tumor repression in prostate cancer xenografts in vivo. Taken together, the present study has demonstrated a previously undefined tumor-suppressing role of CFTR and its involvement in regulation of miR-193b in prostate cancer development.

Indexed as

AnimalsBase SequenceCell Line, TumorCell MovementCystic Fibrosis Transmembrane Conductance RegulatorDown-RegulationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMaleMiceMice, NudeMicroRNAsMolecular Sequence DataProstatic NeoplasmsCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorMicroRNAsMIRN193 microRNA, humanReceptors, Urokinase Plasminogen ActivatorUrokinase-Type Plasminogen Activator

Identifiers

PMID22797075
OpenAlexW2086508420

What OpenQuestion holds

Textmetadata
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.