Evidence map›Paper›PMID 33839456›Full record

ArticleNeoplasia (New York, N.Y.)2021

Role of AMPK and Akt in triple negative breast cancer lung colonization.

Jeremy Johnson, Zeta Chow, Eun Lee, Heidi L Weiss, B Mark Evers, Piotr Rychahou

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  10. Neutrophil Survival Signaling DuringFrontiers in cellular and infection microbiology · 2022
    Article
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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

6 authors at 2 institutions in 1 country.

Jeremy JohnsonDepartment of Toxicology & Cancer Biology, University of Kentucky, Lexington, KY, USA.
Zeta ChowMarkey Cancer Center, Lexington, KY, USA; Department of Surgery, University of Kentucky, KY, USA.
Eun LeeDepartment of Pathology and Laboratory Medicine, University of Kentucky, Lexington, KY, USA.
Heidi L WeissMarkey Cancer Center, Lexington, KY, USA.
B Mark EversMarkey Cancer Center, Lexington, KY, USA; Department of Surgery, University of Kentucky, KY, USA.
Piotr RychahouMarkey Cancer Center, Lexington, KY, USA; Department of Surgery, University of Kentucky, KY, USA. Electronic address: piotr.rychahou@uky.edu.
University of Kentucky · USMarkey Cancer Center · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers · 2013 to 2026
$38.3M
Oncology Research Training for Surgeon-ScientistsT32CA160003 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers, Pamela Carmen Hull · 2011 to 2026
$3.2M
Novel pRNA Nanoparticle Delivery as Directed Therapy for Colorectal Cancer MetastasisR01CA195573 · NCI · UNIVERSITY OF KENTUCKY · PI EVERS, BERNARD MARK, GUO, PEIXUAN · 2015 to 2019
$1.8M
NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA195573NCI NIH HHS T32 CA160003
6 · The paper itself

Abstract

Triple negative breast cancer (TNBC) is an aggressive disease with a 5-y relative survival rate of 11% after distant metastasis. To survive the metastatic cascade, tumor cells remodel their signaling pathways by regulating energy production and upregulating survival pathways. AMP-activated protein kinase (AMPK) and Akt regulate energy homeostasis and survival, however, the individual or synergistic role of AMPK and Akt isoforms during lung colonization by TNBC cells is unknown. The purpose of this study was to establish whether targeting Akt, AMPKα or both Akt and AMPKα isoforms in circulating cancer cells can suppress TNBC lung colonization. Transient silencing of Akt1 or Akt2 dramatically decreased metastatic colonization of lungs by inducing apoptosis or inhibiting invasion, respectively. Importantly, transient pharmacologic inhibition of Akt activity with MK-2206 or AZD5363 inhibitors did not prevent colonization of lung tissue by TNBC cells. Knockdown of AMPKα1, AMPKα2, or AMPKα1/2 also had no effect on metastatic colonization of lungs. Taken together, these findings demonstrate that transient decrease in AMPK isoforms expression alone or in combination with Akt1 in circulating tumor cells does not synergistically reduce TNBC metastatic lung colonization. Our results also provide evidence that Akt1 and Akt2 expression serve as a bottleneck that can challenge colonization of lungs by TNBC cells.

Indexed as

AMP-Activated Protein KinasesAnimalsApoptosisCell Line, TumorEnergy MetabolismFemaleHeterocyclic Compounds, 3-RingHumansLung NeoplasmsMiceMice, Inbred NODMice, SCIDNeoplasm InvasivenessNeoplastic Cells, CirculatingProto-Oncogene Proteins c-aktPyrimidinesAKT1 protein, humanAKT2 protein, humanAMP-Activated Protein KinasescapivasertibHeterocyclic Compounds, 3-RingMK 2206PRKAA1 protein, humanPRKAA2 protein, humanProto-Oncogene Proteins c-aktPyrimidinesPyrrolesRNA, Small InterferingAktAMPKαOrgan metastasisTriple negative breast cancer

Identifiers

PMID33839456
PMCPMC8042649
OpenAlexW3154293384

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.