Evidence map›Paper›PMID 26317663›Full record

ReviewCell cycle (Georgetown, Tex.)2015

Cancer cells exploit adaptive mitochondrial dynamics to increase tumor cell invasion.

M Cecilia Caino, Dario C Altieri

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 40 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

2 authors at 1 institution in 1 country.

M Cecilia Cainoa Prostate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute ; Philadelphia , PA USA.
Dario C Altieria Prostate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute ; Philadelphia , PA USA.
The Wistar Institute · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Maureen E. Murphy · 1985 to 2026
$75.9M
Role of Runx2 in prostate tumorigenesis and metastasisP01CA140043 · NCI · WISTAR INSTITUTE · PI ALTIERI, DARIO C · 2010 to 2021
$12.2M
CONTROL OF APOPTOSIS IN CANCER BY SURVIVINR01CA078810 · NCI · YALE UNIVERSITY · PI ALTIERI, DARIO C · 1998 to 2017
$5.5M
(PQC2) Plasticity Of The.PI3K Network In Early DormancyR01CA190027 · NCI · WISTAR INSTITUTE · PI ALTIERI, DARIO C · 2014 to 2016
$1.2M
Mitochondrial Hsp90s Regulation of Tumor Bioenergetics and MetastasisF32CA177018 · NCI · WISTAR INSTITUTE · PI CAINO, MARIA CECILIA · 2013 to 2015
$171k
NCI NIH HHS CA190027NCI NIH HHS F32 CA177018NCI NIH HHS F32CA177018NCI NIH HHS P01 CA140043NCI NIH HHS P30 CA010815NCI NIH HHS R01 CA078810NCI NIH HHS R01 CA190027NCI NIH HHS R01 CA78810
6 · The paper itself

Abstract

Mitochondria are organelles that orchestrate a plethora of fundamental cellular functions that have been associated with various steps of tumor progression. However, we currently lack a mechanistic understanding of how mitochondrial dynamics, which reflects the organelles' exquisite heterogeneity in shape and spatial distribution, affects tumorigenesis. In a recent study, we uncovered a surprising new role of mitochondrial dynamics in response to PI3K therapy. We found that re-activation of Akt/mTOR signaling in tumor cells exposed to small molecule PI3K antagonists currently in the clinic triggered the transport of energetically active, elongated mitochondria to the cortical cytoskeleton of tumor cells. In turn, these repositioned mitochondria supported increased lamellipodia dynamics, faster turnover of focal adhesion complexes, heightened velocity and distance of random cell migration and increased tumor cell invasion. In this Extra View, we discuss the mechanistic basis of this paradoxical response to PI3K antagonists and propose possible strategies to disable mitochondrial adaptation.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorEnzyme InhibitorsHumansMitochondrial DynamicsNeoplasm InvasivenessNeoplasmsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktAntineoplastic AgentsEnzyme InhibitorsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktdrug resistancefocal adhesionHsp90metastasismitochondriaPI3K

Identifiers

PMID26317663
PMCPMC4825634
OpenAlexW1867774516

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.