Evidence map›Paper›PMID 29341212›Full record

ArticleThe Prostate2018

Differential role of PTEN in transforming growth factor β (TGF-β) effects on proliferation and migration in prostate cancer cells.

Mawiyah N Kimbrough-Allah, Ana C Millena, Shafiq A Khan

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. RETRACTED: PTEN Deficiency Induced by Extracellular Vesicle miRNAs fromInternational journal of molecular sciences · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Alterations in TGFβ signaling during prostate cancer progression.American journal of clinical and experimental urology · 2021
    Review
  12. Review
  13. Article
  14. Review
  15. 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

3 authors at 1 institution in 1 country.

Mawiyah N Kimbrough-AllahCenter for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, Georgia.
Ana C MillenaCenter for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, Georgia.
Shafiq A KhanCenter for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, Georgia.ORCID 0000-0002-1010-313X
Center for Cancer Research · US

Funding

TRAINNING COREP20MD002285 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2007 to 2016
$10.9M
Technologies/Resources for Core LaboratoriesG12MD007590 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2012 to 2018
$7.6M
NIMHD NIH HHS G12 MD007590NIMHD NIH HHS P20 MD002285
6 · The paper itself

Abstract

backgroundTransforming growth factor-β (TGF-β) acts as a tumor suppressor in normal epithelial cells but as a tumor promoter in advanced prostate cancer cells. PI3-kinase pathway mediates TGF-β effects on prostate cancer cell migration and invasion. PTEN inhibits PI3-kinase pathway and is frequently mutated in prostate cancers. We investigated possible role(s) of PTEN in TGF-β effects on proliferation and migration in prostate cancer cells.

methodsExpression of PTEN mRNA and proteins were determined using RT-PCR and Western blotting in RWPE1 and DU145 cells. We also studied the role of PTEN in TGF-β effects on cell proliferation and migration in DU145 cells after transient silencing of endogenous PTEN. Conversely, we determined the role of PTEN in cell proliferation and migration after over-expression of PTEN in PC3 cells which lack endogenous PTEN.

resultsTGF-β1 and TGF-β3 had no effect on PTEN mRNA levels but both isoforms increased PTEN protein levels in DU145 and RWPE1 cells indicating that PTEN may mediate TGF-β effects on cell proliferation. Knockdown of PTEN in DU145 cells resulted in significant increase in cell proliferation which was not affected by TGF-β isoforms. PTEN overexpression in PC3 cells inhibited cell proliferation. Knockdown of endogenous PTEN enhanced cell migration in DU145 cells, whereas PTEN overexpression reduced migration in PC3 cells and reduced phosphorylation of AKT in response to TGF-β.

conclusionWe conclude that PTEN plays a role in inhibitory effects of TGF-β on cell proliferation whereas its absence may enhance TGF-β effects on activation of PI3-kinase pathway and cell migration.

Indexed as

Cell Line, TumorCell MovementCell ProliferationHumansMalePhosphatidylinositol 3-KinasesPhosphorylationProstatic NeoplasmsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRecombinant ProteinsRNA, MessengerTransforming Growth Factor beta1Transforming Growth Factor beta3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanRecombinant ProteinsRNA, MessengerTransforming Growth Factor beta1Transforming Growth Factor beta3cell proliferationmigrationPI3-kinaseprostate cancerPTENTGF-β

Identifiers

PMID29341212
PMCPMC5820153
OpenAlexW2782656955

What OpenQuestion holds

Textmetadata
LicenceTDM
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.