Evidence map›Paper›PMID 30951861›Full record

ArticleCellular signalling2019

The effects of IFITM1 and IFITM3 gene deletion on IFNγ stimulated protein synthesis.

Maria Gómez-Herranz, Marta Nekulova, Jakub Faktor, Lenka Hernychova, Sachin Kote, Elizabeth H Sinclair, Rudolf Nenutil, Borivoj Vojtesek, Kathryn L Ball, Ted R Hupp

Abstract read
In one paragraph

Article in Cellular signalling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

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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

10 authors at 4 institutions in 3 countries.

Maria Gómez-HerranzUniversity of Edinburgh, Institute of Genetics and Molecular Medicine, Edinburgh EH4 2XR, United Kingdom.
Marta NekulovaRegional Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, 656 53 Brno, Czech Republic.
Jakub FaktorRegional Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, 656 53 Brno, Czech Republic.
Lenka HernychovaRegional Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, 656 53 Brno, Czech Republic.
Sachin KoteUniversity of Gdansk, International Centre for Cancer Vaccine Science, Department of Chemistry, Gdansk, Poland.
Elizabeth H SinclairUniversity of Edinburgh, Institute of Genetics and Molecular Medicine, Edinburgh EH4 2XR, United Kingdom.
Rudolf NenutilRegional Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, 656 53 Brno, Czech Republic.
Borivoj VojtesekRegional Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, 656 53 Brno, Czech Republic. Electronic address: vojtesek@mou.cz.
Kathryn L BallUniversity of Edinburgh, Institute of Genetics and Molecular Medicine, Edinburgh EH4 2XR, United Kingdom; Regional Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, 656 53 Brno, Czech Republic. Electronic address: kathryn.ball@ed.ac.uk.
Ted R HuppUniversity of Edinburgh, Institute of Genetics and Molecular Medicine, Edinburgh EH4 2XR, United Kingdom; Regional Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, 656 53 Brno, Czech Republic; University of Gdansk, International Centre for Cancer Vaccine Science, Department of Chemistry, Gdansk, Poland. Electronic address: ted.hupp@ed.ac.uk.
Masaryk Memorial Cancer Institute · CZEdinburgh Cancer Research · GBInstitute of Genetics and Cancer · GBUniversity of Gdańsk · PL

Funding

Biotechnology and Biological Sciences Research Council BB/C511599/1
6 · The paper itself

Abstract

Interferon-induced transmembrane proteins IFITM1 and IFITM3 (IFITM1/3) play a role in both RNA viral restriction and in human cancer progression. Using immunohistochemical staining of FFPE tissue, we identified subgroups of cervical cancer patients where IFITM1/3 protein expression is inversely related to metastasis. Guide RNA-CAS9 methods were used to develop an isogenic IFITM1/IFITM3 double null cervical cancer model in order to define dominant pathways triggered by presence or absence of IFITM1/3 signalling. A pulse SILAC methodology identified IRF1, HLA-B, and ISG15 as the most dominating IFNγ inducible proteins whose synthesis was attenuated in the IFITM1/IFITM3 double-null cells. Conversely, SWATH-IP mass spectrometry of ectopically expressed SBP-tagged IFITM1 identified ISG15 and HLA-B as dominant co-associated proteins. ISG15ylation was attenuated in IFNγ treated IFITM1/IFITM3 double-null cells. Proximity ligation assays indicated that HLA-B can interact with IFITM1/3 proteins in parental SiHa cells. Cell surface expression of HLA-B was attenuated in IFNγ treated IFITM1/IFITM3 double-null cells. SWATH-MS proteomic screens in cells treated with IFITM1-targeted siRNA cells resulted in the attenuation of an interferon regulated protein subpopulation including MHC Class I molecules as well as IFITM3, STAT1, B2M, and ISG15. These data have implications for the function of IFITM1/3 in mediating IFNγ stimulated protein synthesis including ISG15ylation and MHC Class I production in cancer cells. The data together suggest that pro-metastatic growth associated with IFITM1/3 negative cervical cancers relates to attenuated expression of MHC Class I molecules that would support tumor immune escape.

Indexed as

Antigens, DifferentiationCell LineFemaleHistocompatibility Antigens Class IHumansMembrane ProteinsProtein BiosynthesisRNA-Binding ProteinsUterine Cervical NeoplasmsAntigens, DifferentiationHistocompatibility Antigens Class IIFITM3 protein, humanleu-13 antigenMembrane ProteinsRNA-Binding ProteinsCAS9 gene editingCervical cancerIFITM1InterferonMHC Class I moleculeSILAC mass spectrometry

Identifiers

PMID30951861
PMCPMC7111284
OpenAlexW2927006335

What OpenQuestion holds

Textmetadata
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.