Evidence map›Paper›PMID 20672324›Full record

ArticleThe Prostate2011

Inhibition of ADAM9 expression induces epithelial phenotypic alterations and sensitizes human prostate cancer cells to radiation and chemotherapy.

Sajni Josson, Cynthia S Anderson, Shian-Ying Sung, Peter A S Johnstone, Hiroyuki Kubo, Chia-Ling Hsieh, Rebecca Arnold, Murali Gururajan, Clayton Yates, Leland W K Chung

Abstract read
In one paragraph

Article in The Prostate, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.1field-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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  11. ADAM9 Expression in Uterine Cervical Cancer and Its Associated FactorsAsian Pacific journal of cancer prevention : APJCP · 2019
    Article
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  14. The pleiotropic roles of ADAM9 in the biology of solid tumors.Cellular and molecular life sciences : CMLS · 2018
    Review
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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

10 authors at 7 institutions in 3 countries.

Sajni JossonUro-Oncology Research Program, Department of Medicine, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA. sajni.josson@cshs.org
Cynthia S Anderson
Shian-Ying Sung
Peter A S Johnstone
Hiroyuki Kubo
Chia-Ling Hsieh
Rebecca Arnold
Murali Gururajan
Clayton Yates
Leland W K Chung
Cedars-Sinai Medical Center · USEmory University · USCenter for Molecular Medicine and Immunology · USChina Medical University · TWIndiana University Bloomington · USKagoshima University · JPTuskegee University · US

Funding

Prostate Cancer Bone Metastasis: Biology and TargetingP01CA098912 · NCI · EMORY UNIVERSITY · PI ZAYZAFOON, MAJD · 2003 to 2019
$24.0M
Beta 2-Microglobulin signaling and targeting in bone metastasisR01CA122602 · NCI · CEDARS-SINAI MEDICAL CENTER · PI CHUNG, LELAND W.K. · 2009 to 2013
$1.5M
NCI NIH HHS 1R01CA122602NCI NIH HHS 2P01CA098912NCI NIH HHS P01 CA098912NCI NIH HHS R01 CA122602
6 · The paper itself

Abstract

introductionRecent studies demonstrated the importance of ADAM9 in prostate cancer relapse upon therapy. In this study, we determined the role of ADAM9 in the therapeutic resistance to radiation and chemotherapy. MATERIALS AND

methodsADAM9 was either transiently or stably knocked down in C4-2 prostate cancer cells. The sensitivity of ADAM9 knockdown cells toward radiation and chemotherapeutic agents were determined. Additionally, the effects of ADAM9 knockdown on prostate cancer cell morphology, biochemical and functional alterations were accessed.

resultsBoth transient and stable knockdown of ADAM9 resulted in increased apoptosis and increased sensitivity to radiation. ADAM9 knockdown also increased prostate cancer sensitivity to several chemotherapeutic drugs. ADAM9 knockdown resulted in increased E-cadherin and altered integrin expression and underwent phenotypic epithelial transition. These were reflected by the morphological, biochemical, and functional alterations in the ADAM9 knockdown cells.

conclusionsADAM9 plays a crucial role in prostate cancer progression and therapeutic resistance in part by altering E-cadherin and integrin expression. ADAM9 is an important target for the consideration of treating prostate cancer patients who developed therapeutic resistance and disease relapse.

Indexed as

ADAM ProteinsApoptosisCadherinsCell Line, TumorEpitheliumHumansIntegrinsMaleMembrane ProteinsPhenotypeProstatic NeoplasmsRadiation ToleranceSuperoxidesADAM9 protein, humanADAM ProteinsCadherinsIntegrinsMembrane ProteinsSuperoxides

Identifiers

PMID20672324
PMCPMC3174735
OpenAlexW1990107313

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.