Evidence map›Paper›PMID 28656196›Full record

ArticleInternational journal of oncology2017

The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells.

Sanghun Lee, Min Cheol Kwon, Jun-Pil Jang, Jae Kyung Sohng, Hye Jin Jung

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Therapeutic Candidates for Alzheimer's Disease: Saponins.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. [The Effects of Ginsenoside Compound K on PDGF-BB-Induced PASMCs Proliferation and Phenotypic Conversion of Pulmonary Arterial Smooth Muscle Cells].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Article
  9. Article
  10. Article
  11. Anticancer Activities of Ginsenosides, the Main Active Components of Ginseng.Evidence-based complementary and alternative medicine : eCAM · 2021
    Review
  12. Article
  13. Article
  14. Regorafenib and ginsenoside combination therapy: inhibition of HepG2 cell growth through modulating survivin and caspase-3 gene expression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Sanghun LeeDepartment of BT-Convergent Pharmaceutical Engineering, Sun Moon University, Tangjeong-myeon, Asan-si, Chungnam 336-708, Republic of Korea.
Min Cheol KwonAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, Chungbuk 363-883, Republic of Korea.
Jun-Pil JangAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, Chungbuk 363-883, Republic of Korea.
Jae Kyung SohngDepartment of BT-Convergent Pharmaceutical Engineering, Sun Moon University, Tangjeong-myeon, Asan-si, Chungnam 336-708, Republic of Korea.
Hye Jin JungDepartment of BT-Convergent Pharmaceutical Engineering, Sun Moon University, Tangjeong-myeon, Asan-si, Chungnam 336-708, Republic of Korea.
Sun Moon University · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most aggressive and malignant form of primary brain cancer. Despite recent advances in cancer treatment, it remains a substantially incurable disease. Accordingly, more effective GBM therapeutic options are urgently required. In the present study, we investigated the anticancer effect of a ginsenoside metabolite, compound K (CK), against GBM cells. CK significantly inhibited not only growth, but also metastatic ability of U87MG and U373MG cells. CK arrested cell cycle progression at the G0/G1 phase with a decrease in the expression levels of cyclin D1 and cyclin D3 in both cell types. CK also induced apoptosis in GBM cells through nuclear condensation, an increase in ROS generation, mitochondrial membrane potential depolarization, and activation of caspase-3, caspase-9 and poly(ADP-ribose) polymerase (PARP). Furthermore, CK inhibited phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, contributing to the antiproliferative and apoptotic effects. Moreover, CK suppressed the self-renewal capacity as well as the invasiveness of U87MG and U373MG GBM stem-like cells (GSCs) by inducing a reduction in the expression of GSC markers, such as CD133, Nanog, Oct4 and Sox2. Taken together, our findings suggest that CK may potentially be useful for GBM treatment.

Indexed as

ApoptosisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGinsenosidesGlioblastomaHumansNeoplasm ProteinsNeoplastic Stem CellsSignal Transductionginsenoside compound KGinsenosidesNeoplasm Proteins

Identifiers

PMID28656196
PMCPMC5505016
OpenAlexW2654783973

What Socratic 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 Socratic graph.