Evidence map›Paper›PMID 29059164›Full record

ArticleOncogene2018

FAM49B, a novel regulator of mitochondrial function and integrity that suppresses tumor metastasis.

M S Chattaragada, C Riganti, M Sassoe, M Principe, M M Santamorena, C Roux, C Curcio, A Evangelista, P Allavena, R Salvia and 4 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 66 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

14 authors at 3 institutions in 1 country.

M S ChattaragadaDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.
C RigantiDepartment of Oncology, University of Turin, Turin, Italy.ORCID 0000-0001-9787-4836
M SassoeDepartment of Neurosciences, 'Rita Levi Montalcini', University of Turin, Turin, Italy.
M PrincipeDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.
M M SantamorenaDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.
C RouxDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.
C CurcioDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.
A EvangelistaDepartment of Clinical Epidemiology, Azienda Universitaria Ospedaliera Città della Salute e della Scienza and CPO Piemonte, Turin, Italy.
P AllavenaLaboratory of Molecular Gastroenterology, Department of Gastroenterology, Humanitas Clinical and Research Center, Milan, Italy.
R SalviaDepartment of Surgery, The Pancreas Institute, University and Hospital Trust of Verona, Verona, Italy.
B RusevDepartment of Pathology and Public Health & ARC-NET Research Center, University and Hospital Trust of Verona, Verona, Italy.
A ScarpaDepartment of Pathology and Public Health & ARC-NET Research Center, University and Hospital Trust of Verona, Verona, Italy.
P CappelloDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.ORCID 0000-0002-5321-7794
F NovelliDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.ORCID 0000-0002-6259-5666
Azienda Ospedaliera Citta' della Salute e della Scienza di Torino · ITUniversity of Turin · ITHumanitas University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysregulation plays a central role in cancers and drives reactive oxygen species (ROS)-dependent tumor progression. We investigated the pro-tumoral roles of mitochondrial dynamics and altered intracellular ROS levels in pancreatic ductal adenocarcinoma (PDAC). We identified 'family with sequence similarity 49 member B' (FAM49B) as a mitochondria-localized protein that regulates mitochondrial fission and cancer progression. Silencing FAM49B in PDAC cells resulted in increased fission and mitochondrial ROS generation, which enhanced PDAC cell proliferation and invasion. Notably, FAM49B expression levels in PDAC cells were downregulated by the tumor microenvironment. Overall, the results of this study show that FAM49B acts as a suppressor of cancer cell proliferation and invasion in PDAC by regulating tumor mitochondrial redox reactions and metabolism.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAnimalsApoptosisBiomarkers, TumorCarcinoma, Pancreatic DuctalCell MovementCell ProliferationHumansIntracellular Signaling Peptides and ProteinsMiceMice, Inbred NODMice, SCIDMitochondriaMitochondrial ProteinsNeoplasm ProteinsBiomarkers, TumorCYRIB protein, humanIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsNeoplasm ProteinsReactive Oxygen Species

Identifiers

PMID29059164
PMCPMC5808099
OpenAlexW2766516299

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.