Evidence map›Paper›PMID 30419852›Full record

ArticleBMC cancer2018

Epithelial cell adhesion molecule (EpCAM) is involved in prostate cancer chemotherapy/radiotherapy response in vivo.

Jie Ni, Paul Cozzi, Julia Beretov, Wei Duan, Joseph Bucci, Peter Graham, Yong Li

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

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  15. EpCAM as a Novel Biomarker for Survivals in Prostate Cancer Patients.Frontiers in cell and developmental biology · 2022
    Article
  16. Article
  17. Article
  18. Cancer stem cell characteristics and their potential as therapeutic targets.Medical oncology (Northwood, London, England) · 2021
    Review
  19. Article
  20. Preclinical evaluation of radiation therapy ofInternational journal of biological sciences · 2021
    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

7 authors at 3 institutions in 1 country.

Jie NiCancer Care Centre, St George Hospital, Level 2, 4-10 South St, Kogarah, NSW, 2217, Australia.
Paul CozziSt George and Sutherland Clinical School, Faculty of Medicine, UNSW Sydney, Kensington, NSW, 2052, Australia.
Julia BeretovCancer Care Centre, St George Hospital, Level 2, 4-10 South St, Kogarah, NSW, 2217, Australia.
Wei DuanSchool of Medicine and Centre for Molecular and Medical Research, Deakin University, Waurn Ponds, VIC, 3216, Australia.
Joseph BucciCancer Care Centre, St George Hospital, Level 2, 4-10 South St, Kogarah, NSW, 2217, Australia.
Peter GrahamCancer Care Centre, St George Hospital, Level 2, 4-10 South St, Kogarah, NSW, 2217, Australia.
Yong LiCancer Care Centre, St George Hospital, Level 2, 4-10 South St, Kogarah, NSW, 2217, Australia. y.li@unsw.edu.au.
Sutherland Hospital · AUSt George Hospital · AUDeakin University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDevelopment of chemo-/radioresistance is a major challenge for the current prostate cancer (CaP) therapy. We have previously demonstrated that epithelial cell adhesion molecule (EpCAM) is associated with CaP growth and therapeutic resistance in vitro, however, the role of EpCAM in CaP in vivo is not fully elucidated. Here, we aimed to investigate how expression of EpCAM is involved in CaP growth and chemo-/radiotherapy response in NOD/SCID mouse models in vivo and to validate its role as a therapeutic target for CaP therapy.

methodsEpCAM was knocked down in PC-3 CaP cell line using short hairpin RNA (shRNA). The effect of EpCAM-knockdown (KD) on tumour growth, chemo-/radiotherapy response and animal survival was evaluated on subcutaneous (s.c) and orthotopic mouse models.

resultsWe found that KD of EpCAM significantly inhibited tumour growth, increased xenograft sensitivity to chemotherapy/radiotherapy, and prolonged the survival of tumour-bearing mice. In addition, we demonstrated that KD of EpCAM is associated with downregulation of the PI3K/Akt/mTOR pathway.

conclusionsIn conclusion, our data confirms that CaP growth and chemo-/radioresistance in vivo is associated with over-expression of EpCAM, which serves both a functional biomarker and promising therapeutic target.

Indexed as

AnimalsApoptosisCell Line, TumorCell ProliferationChemotherapy, AdjuvantDisease Models, AnimalEpithelial Cell Adhesion MoleculeGene Knockdown TechniquesHumansImmunohistochemistryMaleMiceMice, Inbred NODMice, SCIDNeovascularization, PathologicPhosphatidylinositol 3-KinasesEpithelial Cell Adhesion MoleculeMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Small InterferingTOR Serine-Threonine KinasesAnimal modelChemoresistanceEpCAMPI3K/Akt/mTOR signaling pathwayProstate cancerRadioresistance

Identifiers

PMID30419852
PMCPMC6233586
OpenAlexW2901588705

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.