Evidence map›Paper›PMID 28562340›Full record

ArticleOncotarget2017

Cell type-dependent HIF1 α-mediated effects of hypoxia on proliferation, migration and metastatic potential of human tumor cells.

Enikő Tátrai, Alexandra Bartal, Alexandra Gacs, Sándor Paku, István Kenessey, Tamás Garay, Balázs Hegedűs, Eszter Molnár, Mihály T Cserepes, Zita Hegedűs and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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  14. Review
  15. Selective Inhibition of HIF1α Expression by ZnSOPathology oncology research : POR · 2020
    Article
  16. Hypoxia Alters Epigenetic andFrontiers in oncology · 2020
    Article
  17. Article
  18. High HIF-1α expression predicts poor prognosis of patients with colon adenocarcinoma.International journal of clinical and experimental pathology · 2018
    Article
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

13 authors at 4 institutions in 3 countries.

Enikő TátraiDepartment of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary.
Alexandra BartalDepartment of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary.
Alexandra GacsDepartment of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary.
Sándor Pakust Institute of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.
István Kenesseynd Department of Pathology, Semmelweis University, Budapest, Hungary.
Tamás Garaynd Department of Pathology, Semmelweis University, Budapest, Hungary.
Balázs HegedűsTumor Progression Research Group, Hungarian Academy of Sciences, Semmelweis University, Budapest, Hungary.
Eszter Molnárnd Department of Pathology, Semmelweis University, Budapest, Hungary.
Mihály T CserepesDepartment of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary.
Zita HegedűsDepartment of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary.
Nóra KucsmaInstitute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
Gergely SzakácsInstitute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
József TóváriDepartment of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary.
National Institute of Oncology · HUHungarian Academy of Sciences · HUSemmelweis University · HURuhrlandklinik · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor hypoxia promotes neoangiogenesis and contributes to the radio- and chemotherapy resistant and aggressive phenotype of cancer cells. However, the migratory response of tumor cells and the role of small GTPases regulating the organization of cytoskeleton under hypoxic conditions have yet to be established. Accordingly, we measured the proliferation, migration, RhoA activation, the mRNA and protein levels of hypoxia inducible factor-1alpha (HIF-1α) and three small G-proteins, Rac1, cdc42 and RhoA in a panel of five human tumor cell lines under normoxic and hypoxic conditions. Importantly, HT168-M1 human melanoma cells with high baseline migration capacity showed increased HIF-1α and small GTPases expression, RhoA activation and migration under hypoxia. These activities were blocked by anti- HIF-1α shRNA. Moreover, the in vivo metastatic potential was promoted by hypoxia mimicking CoCl2 treatment and reduced upon inhibition of HIF-1α in a spleen to liver colonization experiment. In contrast, HT29 human colon cancer cells with low migration capacity showed limited response to in vitro hypoxia. The expression of the small G-proteins decreased both at mRNA and protein levels and the RhoA activation was reduced. Nevertheless, the number of lung or liver metastatic colonies disseminating from orthotopic HT29 grafts did not change upon CoCl2 or chetomin treatment. Our data demonstrates that the hypoxic environment induces cell-type dependent changes in the levels and activation of small GTPases and results in varying migratory and metastasis promoting responses in different human tumor cell lines.

Indexed as

Gene ExpressionAnimalsCell HypoxiaCell Line, TumorCell MovementCell ProliferationCytoskeletonDisease Models, AnimalGene SilencingHeterograftsHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMaleMiceNeoplasm MetastasisHypoxia-Inducible Factor 1, alpha SubunitrhoA GTP-Binding ProteinhypoxiametastasisRhoA activationsmall GTPasestumor cell motility

Identifiers

PMID28562340
PMCPMC5546497
OpenAlexW2612102682

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.