Evidence map›Paper›PMID 19190336›Full record

ArticleCancer research2009

Identification of a novel pathway that selectively modulates apoptosis of breast cancer cells.

Alexander A Tinnikov, Kay T Yeung, Sharmistha Das, Herbert H Samuels

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

19 citing papers in PubMed, 46 citations in OpenAlex.

  1. Case Report: NovelFrontiers in immunology · 2025
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  5. Pharmaceuticals (Basel, Switzerland) · 2021
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  14. Identification of a novel fusion gene, IRF2BP2-RARA, in acute promyelocytic leukemia.Journal of the National Comprehensive Cancer Network : JNCCN · 2015
    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

4 authors at 2 institutions in 1 country.

Alexander A TinnikovDepartment of Pharmacology and Medicine, The Entertainment Industry Foundation Research Laboratory, New York University School of Medicine, New York, New York 10016, USA.
Kay T Yeung
Sharmistha Das
Herbert H Samuels
Entertainment Industry Foundation · USNew York University · US

Funding

MEDICAL SCIENTIST TRAININGT32GM007308 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PHILIPS, MARK REID · 1985 to 2019
$23.2M
METABOLIC EFFECTS OF THYROID HORMONE IN CELL CULTURER01DK016636 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SAMUELS, HERBERT H · 1986 to 2007
$6.0M
NIDDK NIH HHS R01 DK016636NIGMS NIH HHS T32 GM007308
6 · The paper itself

Abstract

Expression of the nuclear receptor interacting factor 3 (NRIF3) coregulator in a wide variety of breast cancer cells selectively leads to rapid caspase-2-dependent apoptotic cell death. A novel death domain (DD1) was mapped to a 30-amino acid region of NRIF3. Because the cytotoxicity of NRIF3 and DD1 seems to be cell type-specific, these studies suggest that breast cancer cells contain a novel "death switch" that can be specifically modulated by NRIF3 or DD1. Using an MCF-7 cell cDNA library in a yeast two-hybrid screen, we cloned a factor that mediates apoptosis by DD1 and refer to this factor as DD1-interacting factor-1 (DIF-1). DIF-1 is a transcriptional repressor that mediates its effect through SirT1, and this repression is attenuated by the binding of NRIF3/DD1. DIF-1 expression rescues breast cancer cells from NRIF3/DD1-induced apoptosis. Small interfering RNA (siRNA) knockdown of DIF-1 selectively leads to apoptosis of breast cancer cells, further suggesting that DIF-1 plays a key role in NRIF3/DD1-mediated apoptosis. A protein kinase A inhibitor (H89) also elicits apoptosis of breast cancer cells but not of the other cell types examined, and DIF-1 also protects these cells from H89-mediated apoptosis. In addition, H89 incubation results in a rapid increase in NRIF3 levels and siRNA knockdown of NRIF3 protects breast cancer cells from H89-mediated apoptosis. Our results indicate that DIF-1 plays a key role in breast cancer cell survival and further characterizing this pathway may provide important insights into developing novel therapies to selectively target breast cancer cells for apoptosis.

Indexed as

Alpha-AmanitinApoptosisBreast NeoplasmsCarrier ProteinsCaspase 2Cell DeathCell DivisionCell Line, TumorDNA-Binding ProteinsFemaleHeLa CellsHumansNuclear ProteinsRNA, Small InterferingTranscription FactorsAlpha-AmanitinCarrier ProteinsCaspase 2DNA-Binding ProteinsIRF2BP2 protein, humanITGB3BP protein, humanNuclear ProteinsRNA, Small InterferingTranscription Factors

Identifiers

PMID19190336
PMCPMC4264605
OpenAlexW2122914263

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.