Evidence map›Paper›PMID 36050295›Full record

ArticleCell death & disease2022

Integrated analysis reveals FOXA1 and Ku70/Ku80 as targets of ivermectin in prostate cancer.

Shidong Lv, Zeyu Wu, Mayao Luo, Yifan Zhang, Jianqiang Zhang, Laura E Pascal, Zhou Wang, Qiang Wei

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  8. Re-examining the evidence that ivermectin induces a melanoma-like state in Xenopus embryos.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  9. Article
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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 3 institutions in 2 countries.

Shidong Lv *Department of Urology, Nanfang Hospital, Southern Medical University-Guangzhou, Guangzhou, China.
Zeyu Wu *Department of Urology, University of Pittsburgh School of Medicine-Pittsburgh, Pittsburgh, PA, USA.
Mayao LuoDepartment of Urology, Nanfang Hospital, Southern Medical University-Guangzhou, Guangzhou, China.
Yifan ZhangDepartment of Urology, Nanfang Hospital, Southern Medical University-Guangzhou, Guangzhou, China.
Jianqiang ZhangDepartment of Urology, Nanfang Hospital, Southern Medical University-Guangzhou, Guangzhou, China.
Laura E PascalDepartment of Urology, University of Pittsburgh School of Medicine-Pittsburgh, Pittsburgh, PA, USA.
Zhou WangDepartment of Urology, University of Pittsburgh School of Medicine-Pittsburgh, Pittsburgh, PA, USA. wangz2@upmc.edu.ORCID 0000-0002-1604-4767
Qiang WeiDepartment of Urology, Nanfang Hospital, Southern Medical University-Guangzhou, Guangzhou, China. qwei@smu.edu.cn.ORCID 0000-0001-5925-6922
Nanfang Hospital · CNUniversity of Pittsburgh · USCentral South University · CN

Funding

Cellular mechanisms of androgen action and androgen-response gene EAF2 in prostate cancerR50CA211242 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PASCAL, LAURA ELLEN · 2016 to 2020
$575k
NCI NIH HHS R50 CA211242
6 · The paper itself

Abstract

Ivermectin is a widely used antiparasitic drug and shows promising anticancer activity in various cancer types. Although multiple signaling pathways modulated by ivermectin have been identified in tumor cells, few studies have focused on the exact target of ivermectin. Herein, we report the pharmacological effects and targets of ivermectin in prostate cancer. Ivermectin caused G0/G1 cell cycle arrest, induced cell apoptosis and DNA damage, and decreased androgen receptor (AR) signaling in prostate cancer cells. Further in vivo analysis showed ivermectin could suppress 22RV1 xenograft progression. Using integrated omics profiling, including RNA-seq and thermal proteome profiling, the forkhead box protein A1 (FOXA1) and non-homologous end joining (NHEJ) repair executer Ku70/Ku80 were strongly suggested as direct targets of ivermectin in prostate cancer. The interaction of ivermectin and FOXA1 reduced the chromatin accessibility of AR signaling and the G0/G1 cell cycle regulator E2F1, leading to cell proliferation inhibition. The interaction of ivermectin and Ku70/Ku80 impaired the NHEJ repair ability. Cooperating with the downregulation of homologous recombination repair ability after AR signaling inhibition, ivermectin increased intracellular DNA double-strand breaks and finally triggered cell death. Our findings demonstrate the anticancer effect of ivermectin in prostate cancer, indicating that its use may be a new therapeutic approach for prostate cancer.

Indexed as

Hepatocyte Nuclear Factor 3-alphaIvermectinKu AutoantigenProstatic NeoplasmsAntigens, NuclearDNA Breaks, Double-StrandedDNA End-Joining RepairDNA RepairHumansMaleAntigens, NuclearFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaIvermectinKu Autoantigen

Identifiers

PMID36050295
PMCPMC9436997
OpenAlexW4294086122

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.