Evidence map›Paper›PMID 27534968›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2016

Ankyrin G expression is associated with androgen receptor stability, invasiveness, and lethal outcome in prostate cancer patients.

Tingting Wang, Hatem Abou-Ouf, Samar A Hegazy, Mohammed Alshalalfa, Konstantin Stoletov, John Lewis, Bryan Donnelly, Tarek A Bismar

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  7. Intergenomic signatures of coevolution between Tasmanian devils and an infectious cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

8 authors at 4 institutions in 2 countries.

Tingting WangDepartment of Pathology and Laboratory Medicine, University of Calgary, Calgary Laboratory Services, Calgary, Canada.
Hatem Abou-OufDepartment of Pathology and Laboratory Medicine, University of Calgary, Calgary Laboratory Services, Calgary, Canada.
Samar A HegazyDepartment of Pathology and Laboratory Medicine, University of Calgary, Calgary Laboratory Services, Calgary, Canada.
Mohammed AlshalalfaThe Prostate Cancer Centre, Calgary, AB, Canada.
Konstantin StoletovDepartment of Oncology, University of Alberta, Edmonton, AB, Canada.
John LewisDepartment of Oncology, University of Alberta, Edmonton, AB, Canada.
Bryan DonnellyThe Prostate Cancer Centre, Calgary, AB, Canada.
Tarek A BismarDepartment of Pathology and Laboratory Medicine, University of Calgary, Calgary Laboratory Services, Calgary, Canada. tarek.bismar@cls.ab.ca.
Prostate Cancer Canada · CAUniversity of Alberta · CAUniversity of Calgary · CAZagazig University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ankyrin G (ANK3) is a member of the Ankyrin family, which functions to provide cellular stability by anchoring the cytoskeleton to the plasma membrane. Deregulation of ANK3 expression has been observed in multiple human cancers but its mechanism remains unknown. ANK3 expression in relation to disease progression and patients' outcome was investigated in two cohorts of prostate cancer (PCA). Mechanistic studies were carried out in vitro and in vivo using several PCA cell lines and the avian embryo model. Silencing ANK3 resulted in significant reduction of cell proliferation through an AR-independent mechanism. Decreased ANK3 expression delayed S phase to G2/M cell cycle transition and reduced the expression of cyclins A and B. However, cells with knocked-down ANK3 exhibited significant increase in cell invasion through an AR-dependent mechanism. Furthermore, we found that ANK3 is a regulator of AR protein stability. ANK3 knockdown also promoted cancer cell invasion and extravasations in vivo using the avian embryo model (p < 0.01). In human samples, ANK3 expression was dramatically upregulated in high grade intraepithelial neoplasia (HGPIN) and localized PCA (p < 0.0001). However, it was downregulated castration resistant stage (p < 0.0001) and showed inverse relation to Gleason score (p < 0.0001). In addition, increased expression of ANK3 in cancer tissues was correlated with better cancer-specific survival of PCA patients (p = 0.012). KEY MESSAGE: Silencing ANK3 results in significant reduction of cell proliferation through an AR-independent mechanism. ANK3 knockdown results in significant increase in cell invasion through an AR-dependent mechanism. ANK3 is a regulator of AR protein stability. ANK3 knockdown also promotes cancer cell invasion and extravasation in vivo using the avian embryo model.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAnkyrinsBiological AssayCell CycleCell Line, TumorCell ProliferationChick EmbryoCohort StudiesDisease ProgressionHumansMaleNeoplasm GradingNeoplasm InvasivenessProstateProstatic Intraepithelial NeoplasiaANK3 protein, humanAnkyrinsAR protein, humanReceptors, AndrogenRNA, Small InterferingAndrogen receptorInvasionLethal diseaseMetastasisProgressionProstate cancer

Identifiers

PMID27534968
OpenAlexW2512679781

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.