Evidence map›Paper›PMID 30546365›Full record

ArticleFrontiers in immunology2018

Ginsenoside F1 Promotes Cytotoxic Activity of NK Cells via Insulin-Like Growth Factor-1-Dependent Mechanism.

Hyung-Joon Kwon, Heejae Lee, Go-Eun Choi, Soon Jae Kwon, Ah Young Song, So Jeong Kim, Woo Seon Choi, Sang-Hyun Hwang, Sun Chang Kim, Hun Sik Kim

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2018. 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
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

18 citing papers in PubMed, 32 citations in OpenAlex.

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  12. Therapeutic IGF-I receptor inhibition alters fibrocyte immune phenotype in thyroid-associated ophthalmopathy.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

10 authors at 2 institutions in 1 country.

Hyung-Joon KwonDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
Heejae LeeDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
Go-Eun ChoiDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
Soon Jae KwonDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
Ah Young SongDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
So Jeong KimDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
Woo Seon ChoiDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
Sang-Hyun HwangDepartment of Laboratory Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Sun Chang KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Hun Sik KimDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
Ulsan College · KRCatholic University of Pusan · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ginsenosides are the principal active components of ginseng and are considered attractive candidates for combination cancer therapy because they can kill tumors and have favorable safety profiles. However, the overall benefit of ginsenosides remains unclear, particularly in cancer immunosurveillance, considering the controversial results showing repression or promotion of immune responses. Here we identify a potentiating role of ginsenoside F1 (G-F1) in cancer surveillance by natural killer (NK) cells. Among 15 different ginsenosides, G-F1 most potently enhanced NK cell cytotoxicity in response to diverse activating receptors and cancer cells. G-F1 also improved cancer surveillance in mouse models of lymphoma clearance and metastatic melanoma that rely on NK cell activity. G-F1-treated NK cells exhibited elevated cytotoxic potential such as upregulation of cytotoxic mediators and of activation signals upon stimulation. NK cell potentiation by G-F1 was antagonized by insulin-like growth factor (IGF)-1 blockade and recapitulated by IGF-1 treatment, suggesting the involvement of IGF-1. Thus, our results suggest that G-F1 enhances NK cell function and may have chemotherapeutic potential in NK cell-based immunotherapy. We anticipate our results to be a starting point for further comprehensive studies of ginsenosides in the immune cells mediating cancer surveillance and the development of putative therapeutics.

Indexed as

Killer Cells, NaturalLymphomaNeoplasms, ExperimentalAnimalsGinsenosidesHumansImmunity, CellularImmunotherapyInsulin-Like Growth Factor IMiceginsenoside F1Ginsenosidesinsulin-like growth factor-1, mouseInsulin-Like Growth Factor Icancer surveillancecytotoxicityginsenosideIGF-1natural killer cell

Identifiers

PMID30546365
PMCPMC6279892
OpenAlexW2903351358

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.