Evidence map›Paper›PMID 25704883›Full record

ArticleOncotarget2015

Hydrazinobenzoylcurcumin inhibits androgen receptor activity and growth of castration-resistant prostate cancer in mice.

Min Wu, Sahn-Ho Kim, Indrani Datta, Albert Levin, Gregory Dyson, Jing Li, Stephanie Kaypee, M Mahadeva Swamy, Nilesh Gupta, Ho Jeong Kwon and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.9field-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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
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

13 authors at 4 institutions in 3 countries.

Min WuVattikuti Urology Institute, Henry Ford Hospital, Detroit, MI, USA.
Sahn-Ho KimVattikuti Urology Institute, Henry Ford Hospital, Detroit, MI, USA.
Indrani DattaBioinformatics Core, Public Health Sciences, Henry Ford Hospital, Detroit, MI, USA.
Albert LevinBioinformatics Core, Public Health Sciences, Henry Ford Hospital, Detroit, MI, USA.
Gregory DysonBiostatistics Core, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA.
Jing LiPharmacology Core, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA.
Stephanie KaypeeTranscription and Disease Laboratory, Molecular Biology and Genetics Unit, JNCASR, Bangalore, Karnataka, India.
M Mahadeva SwamyTranscription and Disease Laboratory, Molecular Biology and Genetics Unit, JNCASR, Bangalore, Karnataka, India.
Nilesh GuptaDepartment of Pathology, Henry Ford Hospital, Detroit, MI, USA.
Ho Jeong KwonDepartment of Biotechnology, Translational Research Center for Protein Function Control, Yonsei University, Seoul, Republic of Korea.
Mani MenonVattikuti Urology Institute, Henry Ford Hospital, Detroit, MI, USA.
Tapas K KunduTranscription and Disease Laboratory, Molecular Biology and Genetics Unit, JNCASR, Bangalore, Karnataka, India.
G Prem-Veer ReddyVattikuti Urology Institute, Henry Ford Hospital, Detroit, MI, USA.
Henry Ford Hospital · USJawaharlal Nehru Centre for Advanced Scientific Research · INThe Barbara Ann Karmanos Cancer Institute · USYonsei University · KR

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI PAUL M STEMMER · 1985 to 2026
$68.4M
NCI NIH HHS P30 CA022453
6 · The paper itself

Abstract

There is a critical need for therapeutic agents that can target the amino-terminal domain (NTD) of androgen receptor (AR) for the treatment of castration-resistant prostate cancer (CRPC). Calmodulin (CaM) binds to the AR NTD and regulates AR activity. We discovered that Hydrazinobenzoylcurcumin (HBC), which binds exclusively to CaM, inhibited AR activity. HBC abrogated AR interaction with CaM, suppressed phosphorylation of AR Serine81, and blocked the binding of AR to androgen-response elements. RNA-Seq analysis identified 57 androgen-regulated genes whose expression was significantly (p ≤ 0.002) altered in HBC treated cells as compared to controls. Oncomine analysis revealed that genes repressed by HBC are those that are usually overexpressed in prostate cancer (PCa) and genes stimulated by HBC are those that are often down-regulated in PCa, suggesting a reversing effect of HBC on androgen-regulated gene expression associated with PCa. Ingenuity Pathway Analysis revealed a role of HBC affected genes in cellular functions associated with proliferation and survival. HBC was readily absorbed into the systemic circulation and inhibited the growth of xenografted CRPC tumors in nude mice. These observations demonstrate that HBC inhibits AR activity by targeting the AR NTD and suggest potential usefulness of HBC for effective treatment of CRPC.

Indexed as

AnimalsCell ProliferationCurcuminGene ExpressionHumansMaleMiceMice, NudeNIH 3T3 CellsProstatic Neoplasms, Castration-ResistantPyrazolesRandom AllocationReceptors, AndrogenXenograft Model Antitumor AssaysAR protein, humanCurcuminhydrazinobenzoylcurcuminPyrazolesReceptors, Androgenandrogen receptorcalmodulincastration-resistant prostate cancerCTK7Ahydrazinobenzoylcurcumin

Identifiers

PMID25704883
PMCPMC4467427
OpenAlexW1732138571

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.