Evidence map›Paper›PMID 30664187›Full record

ArticleMolecular medicine reports2019

HepaCAM inhibits cell proliferation and invasion in prostate cancer by suppressing nuclear translocation of the androgen receptor via its cytoplasmic domain.

Qingfu Deng, Li Luo, Zhen Quan, Nanjing Liu, Zhongbo Du, Wei Sun, Chunli Luo, Xiaohou Wu

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. 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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Glial Cell Adhesion Molecule (GlialCAM) Determines Proliferative versus Invasive Cell States in Glioblastoma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Qingfu DengDepartment of Urology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400042, P.R. China.
Li LuoKey Laboratory of Diagnostics Medicine Designated by The Ministry of Education, Chongqing Medical University, Chongqing 400042, P.R. China.
Zhen QuanDepartment of Urology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400042, P.R. China.
Nanjing LiuKey Laboratory of Diagnostics Medicine Designated by The Ministry of Education, Chongqing Medical University, Chongqing 400042, P.R. China.
Zhongbo DuDepartment of Urology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400042, P.R. China.
Wei SunDepartment of Urology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400042, P.R. China.
Chunli LuoKey Laboratory of Diagnostics Medicine Designated by The Ministry of Education, Chongqing Medical University, Chongqing 400042, P.R. China.
Xiaohou WuDepartment of Urology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400042, P.R. China.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocyte cell adhesion molecule (HepaCAM) is a tumour suppressor. However, the mechanism of HepaCAM function in prostate cancer (PCa) remains unknown. In the present study, HepaCAM, androgen receptor (AR) and Ran were analysed in 46 PCa tissue samples using immunohistochemistry. Subsequently, the influence of HepaCAM and its cytoplasmic domain on cell proliferation, migration, and invasion, and associated proteins was examined using MTT, wound healing, Transwell and western blotting assays, respectively. Furthermore, nuclear translocation of AR and Ran was analysed using immunofluorescence and Western blot assays. The results demonstrated that HepaCAM expression was reduced in PCa, and there was an association between downregulation of HepaCAM and changes in the distribution of AR and Ran. Furthermore, HepaCAM, specifically the cytoplasmic domain, was involved in cell proliferation, migration and invasion. Nuclear translocation of AR was dependent on HepaCAM and its cytoplasmic domain. Additionally, HepaCAM suppression of the nuclear translocation of AR occurred via Ran. The results suggest that HepaCAM and its cytoplasmic domain suppress the nuclear translocation of AR via Ran in PCa. The cytoplasmic domain of HepaCAM may serve as a novel target for therapy in PCa.

Indexed as

Active Transport, Cell NucleusCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMaleProstatic NeoplasmsProtein DomainsProteinsran GTP-Binding ProteinReceptors, AndrogenSignal TransductionAR protein, humanCell Cycle ProteinsHEPACAM protein, humanProteinsran GTP-Binding ProteinRAN protein, humanReceptors, Androgen

Identifiers

PMID30664187
PMCPMC6390061
OpenAlexW2910664553

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.