Evidence map›Paper›PMID 24905002›Full record

ArticlePloS one2014

Dormancy of cancer cells with suppression of AKT activity contributes to survival in chronic hypoxia.

Hiroko Endo, Hiroaki Okuyama, Masayuki Ohue, Masahiro Inoue

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
1.8field-weighted citation impact, top 16% 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, 59 citations in OpenAlex.

  1. Article
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  9. Cancer Cell Dormancy in the Bone Microenvironment.Current osteoporosis reports · 2025
    Review
  10. Review
  11. Colorectal cancer cell dormancy: An insight into pathways.World journal of gastroenterology · 2024
    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

4 authors at 1 institution in 1 country.

Hiroko EndoDepartment of Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan.
Hiroaki OkuyamaDepartment of Pathology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan.
Masayuki OhueDepartment of Surgery, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan.
Masahiro InoueDepartment of Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan.
Osaka Medical Center for Cancer and Cardiovascular Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A hypoxic microenvironment in tumors has been recognized as a cause of malignancy or resistance to various cancer therapies. In contrast to recent progress in understanding the acute response of cancer cells to hypoxia, the characteristics of tumor cells in chronic hypoxia remain elusive. We have identified a pancreatic cancer cell line, AsPC-1, that is exceptionally able to survive for weeks under 1% oxygen conditions while most tested cancer cell lines die after only some days under these conditions. In chronic hypoxia, AsPC-1 cells entered a state of dormancy characterized by no proliferation, no death, and metabolic suppression. They reversibly switched to active status after being placed again in optimal culture conditions. ATP turnover, an indicator of energy demand, was markedly decreased and accompanied by reduced AKT phosphorylation. Forced activation of AKT resulted in increased ATP turnover and massive cell death in vitro and a decreased number of dormant cells in vivo. In contrast to most cancer cell lines, primary-cultured colorectal cancer cells easily entered the dormant status with AKT suppression under hypoxia combined with growth factor-depleted conditions. Primary colorectal cancer cells in dormancy were resistant to chemotherapy. Thus, the ability to survive in a deteriorated microenvironment by entering into dormancy under chronic hypoxia might be a common property among cancer cells. Targeting the regulatory mechanism inducing this dormant status could provide a new strategy for treating cancer.

Indexed as

Tumor MicroenvironmentCell HypoxiaCell Line, TumorCell SurvivalColorectal NeoplasmsDown-RegulationDrug Resistance, NeoplasmEnergy MetabolismEnzyme ActivationHumansHypoxia-Inducible Factor 1, alpha SubunitIntercellular Signaling Peptides and ProteinsIntracellular SpacePancreatic NeoplasmsPhosphorylationProto-Oncogene Proteins c-aktHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIntercellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID24905002
PMCPMC4048292
OpenAlexW2117971476

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.