Evidence map›Paper›PMID 25161875›Full record

ArticleFEBS open bio2014

Discovery of Sanggenon G as a natural cell-permeable small-molecular weight inhibitor of X-linked inhibitor of apoptosis protein (XIAP).

Maximilian A Seiter, Stefan Salcher, Martina Rupp, Judith Hagenbuchner, Ursula Kiechl-Kohlendorfer, Jérémie Mortier, Gerhard Wolber, Judith M Rollinger, Petra Obexer, Michael J Ausserlechner

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

2 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. 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

10 authors at 4 institutions in 2 countries.

Maximilian A SeiterDepartment of Pediatrics I, Medical University Innsbruck, Anichstraße 35, A-6020 Innsbruck, Austria ; Tyrolean Cancer Research Institute, Innrain 66, A-6020 Innsbruck, Austria.
Stefan SalcherDepartment of Pediatrics II, Medical University Innsbruck, Anichstraße 35, A-6020 Innsbruck, Austria ; Tyrolean Cancer Research Institute, Innrain 66, A-6020 Innsbruck, Austria.
Martina RuppDepartment of Pediatrics II, Medical University Innsbruck, Anichstraße 35, A-6020 Innsbruck, Austria ; Tyrolean Cancer Research Institute, Innrain 66, A-6020 Innsbruck, Austria.
Judith HagenbuchnerDepartment of Pediatrics II, Medical University Innsbruck, Anichstraße 35, A-6020 Innsbruck, Austria ; Tyrolean Cancer Research Institute, Innrain 66, A-6020 Innsbruck, Austria.
Ursula Kiechl-KohlendorferDepartment of Pediatrics II, Medical University Innsbruck, Anichstraße 35, A-6020 Innsbruck, Austria.
Jérémie MortierFreie Universität Berlin, Institute of Pharmacy, Department Pharmaceutical & Medicinal Chemistry, Koenigin-Luise-Straße 2, 14195 Berlin, Germany.
Gerhard WolberFreie Universität Berlin, Institute of Pharmacy, Department Pharmaceutical & Medicinal Chemistry, Koenigin-Luise-Straße 2, 14195 Berlin, Germany.
Judith M RollingerInstitutes of Pharmacy/Pharmacognosy and Center for Molecular Biosciences Innsbruck, University of Innsbruck, Innrain 80-82, A-6020 Innsbruck, Austria.
Petra ObexerDepartment of Pediatrics II, Medical University Innsbruck, Anichstraße 35, A-6020 Innsbruck, Austria ; Tyrolean Cancer Research Institute, Innrain 66, A-6020 Innsbruck, Austria.
Michael J AusserlechnerDepartment of Pediatrics I, Medical University Innsbruck, Anichstraße 35, A-6020 Innsbruck, Austria ; Tyrolean Cancer Research Institute, Innrain 66, A-6020 Innsbruck, Austria.
Tyrolean Cancer Research Institute · ATFreie Universität Berlin · DEInnsbruck Medical University · ATUniversität Innsbruck · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defects in the regulation of apoptosis are one main cause of cancer development and may result from overexpression of anti-apoptotic proteins such as the X-linked inhibitor of apoptosis protein (XIAP). XIAP is frequently overexpressed in human leukemia and prostate and breast tumors. Inhibition of apoptosis by XIAP is mainly coordinated through direct binding to the initiator caspase-9 via its baculovirus-IAP-repeat-3 (BIR3) domain. XIAP inhibits caspases directly making it to an attractive target for anti-cancer therapy. In the search for novel, non-peptidic XIAP inhibitors in this study we focused on the chemical constituents of sāng bái pí (mulberry root bark). Most promising candidates of this plant were tested biochemically in vitro by a fluorescence polarization (FP) assay and in vivo via protein fragment complementation analysis (PCA). We identified the Diels Alder adduct Sanggenon G (SG1) as a novel, small-molecular weight inhibitor of XIAP. As shown by FP and PCA analyses, SG1 binds specifically to the BIR3 domain of XIAP with a binding affinity of 34.26 μM. Treatment of the transgenic leukemia cell line Molt3/XIAP with SG1 enhances caspase-8, -3 and -9 cleavage, displaces caspase-9 from XIAP as determined by immunoprecipitation experiments and sensitizes these cells to etoposide-induced apoptosis. SG1 not only sensitizes the XIAP-overexpressing leukemia cell line Molt3/XIAP to etoposide treatment but also different neuroblastoma cell lines endogenously expressing high XIAP levels. Taken together, Sanggenon G (SG1) is a novel, natural, non-peptidic, small-molecular inhibitor of XIAP that can serve as a starting point to develop a new class of improved XIAP inhibitors.

Indexed as

ARPF-FAM, ARPF-K(5-Fam)-NH2-peptideBIR-3, baculovirus-IAP-repeat-3CC, column chromatographyCell permeable(FP-) assay, fluorescence polarization assayKd, dissociation constantKi, binding affinityMAC, methanol crude extract of mulberry root barkNaturalPCA, protein fragment complementation analysisRLU, relative luminescence unitsSanggenon GSG1, sanggenon GSmall-molecular weightXIAP inhibitorXIAP, X-linked inhibitor of apoptosis protein

Identifiers

PMID25161875
PMCPMC4141193
OpenAlexW2077410013

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.