Evidence map›Paper›PMID 26873959›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016

Identification of Niclosamide as a Novel Anticancer Agent for Adrenocortical Carcinoma.

Kei Satoh, Lisa Zhang, Yaqin Zhang, Raju Chelluri, Myriem Boufraqech, Naris Nilubol, Dhaval Patel, Min Shen, Electron Kebebew

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
10.0field-weighted citation impact, top 1% 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

61 citing papers in PubMed, 97 citations in OpenAlex.

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1 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Kei SatohEndocrine Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland. Icahn School of Medicine at Mount Sinai, New York, New York.
Lisa ZhangEndocrine Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland.
Yaqin ZhangDivision of Pre-Clinical Innovation, National Center for Advancing Translational Sciences, NIH, Bethesda, Maryland.
Raju ChelluriSUNY Upstate Medical University at Syracuse, Syracuse, New York.
Myriem BoufraqechEndocrine Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland.
Naris NilubolEndocrine Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland.
Dhaval PatelEndocrine Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland.
Min ShenDivision of Pre-Clinical Innovation, National Center for Advancing Translational Sciences, NIH, Bethesda, Maryland.
Electron KebebewEndocrine Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland. kebebewe@mail.nih.gov.
Icahn School of Medicine at Mount Sinai · US

Funding

Small molecule screening programZ01HG200319 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI AUSTIN, CHRISTOPHER P · 2004 to 2008
$32.3M
Therapeutic targets and novel anticancer agents for endocrine cancersZIABC011286 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NILUBOL, NARIS · 2010 to 2025
$16.6M
Howard Hughes Medical InstituteIntramural NIH HHS Z01 HG200319Intramural NIH HHS ZIA BC011286
6 · The paper itself

Abstract

purposeAdrenocortical carcinoma (ACC) is a rare and aggressive cancer, and no current effective therapy is available for locally advanced and metastatic ACC. Drug repurposing is an emerging approach for identifying new indications for existing drugs, especially for rare cancers such as ACC. The objective of this study was to use quantitative high-throughput screening to identify agents with antineoplastic activity against ACC. EXPERIMENTAL

designA screening of 4,292 compounds was performed on three ACC cell lines: BD140A, SW-13, and NCI-H295R.

resultsTwenty-one active compounds were identified, with an efficacy of >80% in all three cell lines. Of these, niclosamide showed higher efficacy and lower IC50 than established anti-ACC drugs. We then validated niclosamide-inhibited cellular proliferation in all three ACC cell lines. Next, we investigated the mechanism by which niclosamide inhibited ACC cell proliferation, and found that it induced caspase-dependent apoptosis and G1 cell-cycle arrest. Niclosamide also decreased cellular migration and reduced the level of mediators of epithelial-to-mesenchymal transition, such as N-cadherin and vimentin. Furthermore, niclosamide treatment resulted in decreased expression of β-catenin. We also evaluated the effect of niclosamide on energy metabolism in ACC cell lines and found it resulted in mitochondrial uncoupling. Niclosamide treatment inhibited ACC tumor growth with no observed toxicity in mice in vivo

conclusionsOur findings suggest that niclosamide has anti-ACC activity through its inhibition of multiple altered cellular pathways and cellular metabolism in ACC. Our results provide a preclinical rationale for evaluating niclosamide therapy in a clinical trial for ACC. Clin Cancer Res; 22(14); 3458-66. ©2016 AACR.

Indexed as

Adrenal Cortex NeoplasmsAdrenocortical CarcinomaAnimalsAntineoplastic AgentsApoptosisbeta CateninCadherinsCaspasesCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionG1 PhaseGene Expression Regulation, NeoplasticHumansAntineoplastic Agentsbeta CateninCadherinsCaspasesNiclosamide

Identifiers

PMID26873959
PMCPMC4947455
OpenAlexW2263228961

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.