Evidence map›Paper›PMID 28411130›Full record

ArticleCancer letters2017

IFITM1 suppression blocks proliferation and invasion of aromatase inhibitor-resistant breast cancer in vivo by JAK/STAT-mediated induction of p21.

Asona J Lui, Eric S Geanes, Joshua Ogony, Fariba Behbod, Jordan Marquess, Kelli Valdez, William Jewell, Ossama Tawfik, Joan Lewis-Wambi

Open access · bronzeAbstract read
In one paragraph

Article in Cancer letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 51 citations in OpenAlex.

  1. Predictive model for clear cell renal cell carcinoma: a novel model integrating sunitinib resistance and prognosis related genes and clinical factors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  15. Combined loss of CDH1 and downstream regulatory sequences drive early-onset diffuse gastric cancer and increase penetrance of hereditary diffuse gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
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  18. Estrogen Receptors-Mediated Apoptosis in Hormone-Dependent Cancers.International journal of molecular sciences · 2022
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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

9 authors at 3 institutions in 1 country.

Asona J LuiDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, USA; The University of Kansas Cancer Center, Kansas City, KS 66160, USA. Electronic address: alui@kumc.edu.
Eric S GeanesDepartment of Cancer Biology, University of Kansas Medical Center, USA; The University of Kansas Cancer Center, Kansas City, KS 66160, USA. Electronic address: egeanes@kumc.edu.
Joshua OgonyDepartment of Cancer Biology, University of Kansas Medical Center, USA; The University of Kansas Cancer Center, Kansas City, KS 66160, USA. Electronic address: jogony@kumc.edu.
Fariba BehbodDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, USA; The University of Kansas Cancer Center, Kansas City, KS 66160, USA. Electronic address: fbehbod@kumc.edu.
Jordan MarquessUniversity of Kansas Medical Center School of Medicine, USA. Electronic address: jmarquess@kumc.edu.
Kelli ValdezDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, USA; The University of Kansas Cancer Center, Kansas City, KS 66160, USA. Electronic address: kvaldez@kumc.edu.
William JewellThe University of Kansas Cancer Center, Kansas City, KS 66160, USA. Electronic address: wjewell@kumc.edu.
Ossama TawfikDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, USA. Electronic address: otawfik@kumc.edu.
Joan Lewis-WambiDepartment of Cancer Biology, University of Kansas Medical Center, USA; The University of Kansas Cancer Center, Kansas City, KS 66160, USA. Electronic address: jlewis-wambi@kumc.edu.
The University of Kansas Cancer Center · USUniversity Medical Center · USUniversity of Kansas Medical Center · US

Funding

Transgenic & Gene-Targeting Shared ResourceP30CA168524 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ROY A. JENSEN · 2012 to 2026
$40.1M
Transgenic and Gener-Targeting CoreP20GM104936 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SAADI, IRFAN · 2012 to 2016
$10.9M
Novel Approaches for the Control of Microbial PathogensP30GM103326 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUTKENHAUS, JOSEPH F · 2012 to 2016
$5.3M
Identifying the Molecular and Cellular Basis of Invasive Phenotype in Human DCISR01CA207445 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BEHBOD, FARIBA · 2017 to 2019
$1.7M
The new biology of estrogen action in aromatase resistance breast cancer cellsK01CA120051 · NCI · FOX CHASE CANCER CENTER · PI LEWIS-WAMBI, JOAN SUEDEE · 2007 to 2011
$628k
Role of IFN inducible transmembrane protein 1 in AI-resistant breast cancerF30CA203160 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUI, ASONA J · 2016 to 2019
$117k
NCI NIH HHS F30 CA203160NCI NIH HHS K01 CA120051NCI NIH HHS P30 CA168524NCI NIH HHS R01 CA207445NIGMS NIH HHS P20 GM104936NIGMS NIH HHS P30 GM103326
6 · The paper itself

Abstract

Interferon induced transmembrane protein 1 (IFITM1) belongs to a family of interferon stimulated genes (ISGs) that is associated with tumor progression and DNA damage resistance; however, its role in endocrine resistance is not known. Here, we correlate IFITM1 expression with clinical stage and poor response to endocrine therapy in a tissue microarray consisting of 94 estrogen receptor (ER)-positive breast tumors. IFITM1 overexpression is confirmed in the AI-resistant MCF-7:5C cell line and not found in AI-sensitive MCF-7 cells. In this study, the orthotopic (mammary fat pad) and mouse mammary intraductal (MIND) models of breast cancer are used to assess tumor growth and invasion in vivo. Lentivirus-mediated shRNA knockdown of IFITM1 in AI-resistant MCF-7:5C cells diminished tumor growth and invasion and induced cell death, whereas overexpression of IFITM1 in wild-type MCF-7 cells promoted estrogen-independent growth and enhanced their aggressive phenotype. Mechanistic studies indicated that loss of IFITM1 in MCF-7:5C cells markedly increased p21 transcription, expression and nuclear localization which was mediated by JAK/STAT activation. These findings suggest IFITM1 overexpression contributes to breast cancer progression and that targeting IFITM1 may be therapeutically beneficial to patients with endocrine-resistant disease.

Indexed as

Drug Resistance, NeoplasmAdultAgedAged, 80 and overAnimalsAntigens, DifferentiationAntineoplastic Agents, HormonalAromatase InhibitorsBreast NeoplasmsCell MovementCell ProliferationCyclin-Dependent Kinase Inhibitor p21Down-RegulationEnzyme ActivationFemaleGene Expression Regulation, NeoplasticAntigens, DifferentiationAntineoplastic Agents, HormonalAromatase InhibitorsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Janus Kinasesleu-13 antigenSTAT1 protein, humanSTAT1 Transcription FactorAromatase inhibitor-resistanceInterferon stimulated genesJAK/STAT signalingMouse mammary intraductal modelp21

Identifiers

PMID28411130
PMCPMC5530765
OpenAlexW2606408132

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.