Evidence map›Paper›PMID 27105540›Full record

ArticleOncotarget2016

The Arf-like GTPase Arl8b is essential for three-dimensional invasive growth of prostate cancer in vitro and xenograft formation and growth in vivo.

Samantha S Dykes, Alana L Gray, David T Coleman, Madhurima Saxena, Charles A Stephens, Jennifer L Carroll, Kevin Pruitt, James A Cardelli

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.6field-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

43 citing papers in PubMed, 63 citations in OpenAlex.

  1. BORC assemblies integrate BLOC-1 subunits to diversify endosomal trafficking functions.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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 2 institutions in 1 country.

Samantha S DykesDepartment of Microbiology and Immunology, LSU Health Shreveport, Shreveport, LA, USA.
Alana L GrayDepartment of Microbiology and Immunology, LSU Health Shreveport, Shreveport, LA, USA.
David T ColemanDepartment of Microbiology and Immunology, LSU Health Shreveport, Shreveport, LA, USA.
Madhurima SaxenaFeist-Weiller Cancer Center, LSU Health Shreveport, Shreveport, LA, USA.
Charles A StephensDepartment of Microbiology and Immunology, LSU Health Shreveport, Shreveport, LA, USA.
Jennifer L CarrollDepartment of Microbiology and Immunology, LSU Health Shreveport, Shreveport, LA, USA.
Kevin PruittFeist-Weiller Cancer Center, LSU Health Shreveport, Shreveport, LA, USA.
James A CardelliDepartment of Microbiology and Immunology, LSU Health Shreveport, Shreveport, LA, USA.
Louisiana State University Health Sciences Center Shreveport · USTexas Tech University Health Sciences Center · US

Funding

Mechanisms of Epigenetic Gene SilencingR01CA155223 · NCI · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI PRUITT, KEVIN · 2011 to 2015
$1.4M
NCI NIH HHS R01 CA155223
6 · The paper itself

Abstract

Cancer is a multistep process that requires cells to respond appropriately to the tumor microenvironment, both in early proliferative stages and in later invasive disease. Arl8b is a lysosome localized Arf-like GTPase that controls the spatial distribution of lysosomes via recruitment of kinesin motors. Common features of the tumor microenvironment such as acidic extracellular pH and various growth factors stimulate lysosome trafficking to the cell periphery (anterograde), which is critical for tumor invasion by facilitating the release of lysosomal proteases to promote matrix remodeling. Herein we report for the first time that Arl8b regulates anterograde lysosome trafficking in response to hepatocyte growth factor, epidermal growth factor, and acidic extracellular pH. Depletion of Arl8b results in juxtanuclear lysosome aggregation, and this effect corresponds with both diminished invasive growth and proteolytic extracellular matrix degradation in a three-dimensional model of prostate cancer. Strikingly, we found that depletion of Arl8b abolishes the ability of prostate cancer cells to establish subcutaneous xenografts in mice. We present evidence that Arl8b facilitates lipid hydrolysis to maintain efficient metabolism for a proliferative capacity in low nutrient environments, suggesting a likely explanation for the complete inability of Arl8b-depleted tumor cells to grow in vivo. In conclusion, we have identified two mechanisms by which Arl8b regulates cancer progression: 1) through lysosome positioning and protease release leading to an invasive phenotype and 2) through control of lipid metabolism to support cellular proliferation. These novel roles highlight that Arl8b is a potential target for the development of novel anti-cancer therapeutics.

Indexed as

ADP-Ribosylation FactorsAnimalsCell Growth ProcessesCell Line, TumorHeterograftsHumansMaleMiceMice, SCIDNeoplasm InvasivenessProstatic NeoplasmsSignal TransductionADP-Ribosylation FactorsARL8B protein, humanArl8binvasionlipid metabolismlysosomexenograft

Identifiers

PMID27105540
PMCPMC5058737
OpenAlexW2339061544

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.