Evidence map›Paper›PMID 32493957›Full record

ArticleOncogene2020

BIF-1 inhibits both mitochondrial and glycolytic ATP production: its downregulation promotes melanoma growth.

Živa Frangež, Yuniel Fernández-Marrero, Darko Stojkov, S Morteza Seyed Jafari, Robert E Hunger, Valentin Djonov, Carsten Riether, Hans-Uwe Simon

Abstract read
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Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 12 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

8 authors at 1 institution in 2 countries.

Živa FrangežInstitute of Pharmacology, University of Bern, Bern, Switzerland.
Yuniel Fernández-MarreroInstitute of Pharmacology, University of Bern, Bern, Switzerland.
Darko StojkovInstitute of Pharmacology, University of Bern, Bern, Switzerland.
S Morteza Seyed JafariDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.ORCID http://orcid.org/0000-0002-6466-2199
Robert E HungerDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Valentin DjonovInstitute of Anatomy, University of Bern, Bern, Switzerland.
Carsten RietherTumor Immunology, Department for Biomedical Research, University of Bern, Bern, Switzerland.ORCID http://orcid.org/0000-0001-7512-513X
Hans-Uwe SimonInstitute of Pharmacology, University of Bern, Bern, Switzerland. hus@pki.unibe.ch.ORCID http://orcid.org/0000-0002-9404-7736
University of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endophilin B1, also known as BAX-interacting protein 1 (BIF-1), is part of the endophilin B protein family, and is a multifunctional protein involved in the regulation of apoptosis, autophagy, and mitochondrial morphology. The role of BIF-1 in cancer is controversial since previous reports indicated to both tumor-promoting and tumor-suppressive roles, perhaps depending on the cancer cell type. In the present study, we report that BIF-1 is significantly downregulated in both primary and metastatic melanomas, and that patients with high levels of BIF-1 expression exhibited a better overall survival. Depleting BIF-1 using CRISPR/Cas9 technology in melanoma cells resulted in higher proliferation rates both in vitro and in vivo, a finding that was associated with increased ATP production, metabolic acidification, and mitochondrial respiration. We also observed mitochondrial hyperpolarization, but no increase in the mitochondrial content of BIF-1-knockout melanoma cells. In contrast, such knockout melanoma cells were equally sensitive to anticancer drug- or UV irradiation-induced cell death, and exhibited similar autophagic activities as compared with control cells. Taken together, it appears that downregulation of BIF-1 contributes to tumorigenesis in cutaneous melanoma by upregulating mitochondrial respiration and metabolism, independent of its effect on apoptosis and autophagy.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAdenosine TriphosphateAnimalsApoptosisAutophagyCell Line, TumorDown-RegulationGlycolysisHumansKaplan-Meier EstimateMelanomaMice, Inbred NODMice, KnockoutMice, SCIDMitochondriaAdaptor Proteins, Signal TransducingAdenosine TriphosphateSH3GLB1 protein, human

Identifiers

PMID32493957
OpenAlexW3030118658

What OpenQuestion holds

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Registered trials

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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.