Evidence map›Paper›PMID 24452734›Full record

ArticleScientific reports2014

HIF-1-mediated metabolic reprogramming reduces ROS levels and facilitates the metastatic colonization of cancers in lungs.

Tao Zhao, Yuxi Zhu, Akiyo Morinibu, Minoru Kobayashi, Kazumi Shinomiya, Satoshi Itasaka, Michio Yoshimura, Guozheng Guo, Masahiro Hiraoka, Hiroshi Harada

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.7field-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

65 citing papers in PubMed, 116 citations in OpenAlex.

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5 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 2 countries.

Tao Zhao1] Group of Radiation and Tumor Biology, Department of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine. 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan [2] Group of Radiation and Tumor Biology, Career-Path Promotion Unit for Young Life Scientists, Kyoto University. Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan [3] Department of Radiation Medicine, Fourth Military Medical University. 17 Changle West Road, Xi'an, Shaanxi 710032, China.
Yuxi Zhu1] Group of Radiation and Tumor Biology, Department of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine. 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan [2] Group of Radiation and Tumor Biology, Career-Path Promotion Unit for Young Life Scientists, Kyoto University. Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan [3] Department of Oncology, The First Affiliated Hospital of Chongqing Medical University. No.1 Friendship Road, Yuanjiagang, Yuzhong District, Chongqing 400016, China.
Akiyo Morinibu1] Group of Radiation and Tumor Biology, Department of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine. 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan [2] Group of Radiation and Tumor Biology, Career-Path Promotion Unit for Young Life Scientists, Kyoto University. Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Minoru Kobayashi1] Group of Radiation and Tumor Biology, Department of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine. 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan [2] Group of Radiation and Tumor Biology, Career-Path Promotion Unit for Young Life Scientists, Kyoto University. Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Kazumi Shinomiya1] Group of Radiation and Tumor Biology, Department of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine. 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan [2] Group of Radiation and Tumor Biology, Career-Path Promotion Unit for Young Life Scientists, Kyoto University. Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Satoshi ItasakaGroup of Radiation and Tumor Biology, Department of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine. 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Michio YoshimuraGroup of Radiation and Tumor Biology, Department of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine. 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Guozheng GuoDepartment of Radiation Medicine, Fourth Military Medical University. 17 Changle West Road, Xi'an, Shaanxi 710032, China.
Masahiro HiraokaGroup of Radiation and Tumor Biology, Department of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine. 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Hiroshi Harada1] Group of Radiation and Tumor Biology, Department of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine. 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan [2] Group of Radiation and Tumor Biology, Career-Path Promotion Unit for Young Life Scientists, Kyoto University. Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Kyoto University · JPAir Force Medical University · CNChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia-inducible factor 1 (HIF-1) has been associated with distant tumor metastasis; however, its function in multiple metastatic processes has not yet been fully elucidated. In the present study, we demonstrated that cancer cells transiently upregulated HIF-1 activity during their metastatic colonization after extravasation in the lungs in hypoxia-independent and reactive oxygen species (ROS)-dependent manners. Transient activation induced the expression of lactate dehydrogenase A and phosphorylation of the E1α subunit of pyruvate dehydrogenase, which indicated the reprogramming of glucose metabolic pathways from mitochondrial oxidative phosphorylation to anaerobic glycolysis and lactic acid fermentation. The administration of the HIF-1 inhibitor, YC-1, inhibited this reprogramming, increased intratumoral ROS levels, and eventually suppressed the formation of metastatic lung tumors. These results indicate that HIF-1-mediated metabolic reprogramming is responsible for the survival of metastatic cancers during their colonization in lungs by reducing cytotoxic ROS levels; therefore, its blockade by HIF-1-inhibitors is a rational strategy to prevent tumor metastasis.

Indexed as

AnaerobiosisAnimalsFemaleGlucoseGlycolysisHypoxia-Inducible Factor 1Immunoenzyme TechniquesLactic AcidLung NeoplasmsMammary Neoplasms, ExperimentalMiceMice, NudeMitochondriaOxidative PhosphorylationReactive Oxygen SpeciesSignal TransductionGlucoseHypoxia-Inducible Factor 1Lactic AcidReactive Oxygen Species

Identifiers

PMID24452734
PMCPMC3899644
OpenAlexW1993739517

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.