Evidence map›Paper›PMID 33000213›Full record

ArticleInternational journal of molecular medicine2020

Ginsenoside Rh2 inhibits HeLa cell energy metabolism and induces apoptosis by upregulating voltage‑dependent anion channel 1.

Ying Liu, Jiawen Wang, Juhui Qiao, Shichao Liu, Siming Wang, Daqing Zhao, Xueyuan Bai, Meichen Liu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Ginsenosides on stem cells fate specification-a novel perspective.Frontiers in cell and developmental biology · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Effect of Increased IL-1β on Expression of HK in Alzheimer's Disease.International journal of molecular sciences · 2021
    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

8 authors at 1 institution in 1 country.

Ying LiuJilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.
Jiawen WangJilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.
Juhui QiaoJilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.
Shichao LiuAcademic Affairs Office, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.
Siming WangJilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.
Daqing ZhaoJilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.
Xueyuan BaiJilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.
Meichen LiuJilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.
Changchun University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

20(S)‑Ginsenoside Rh2 [20(S)‑GRh2], one of the main active components of Panax ginseng, induces apoptosis in a wide range of cancer cell types. The present study found that 20(S)‑GRh2 reduces mitochondrial membrane potential, decreases adenosine triphosphate generation and induces reactive oxygen species in HeLa cervical cancer cells. In addition, 20(S)‑GRh2 activated mitochondrion‑dependent apoptosis and inhibited both mitochondrial oxidative phosphorylation and glycolysis in HeLa cells. It was found that voltage‑dependent anion channel 1 (VDAC1) expression was significantly upregulated by 20(S)‑GRh2 treatment, while hexokinase 2 expression was downregulated and segregated from the mitochondria. Furthermore, 20(S)‑GRh2 promoted Bax transport from the cytoplasm to the mitochondria, and knockdown of VDAC1 inhibited Bax transport and apoptosis. These results suggest that VDAC1 is a novel target of 20(S)‑GRh2. The present study provides a better understanding of the mechanistic link between cervical cancer metabolism and growth control, and these results may facilitate the development of new treatments for cervical cancer.

Indexed as

Adenosine TriphosphateApoptosisbcl-2-Associated X ProteinCell RespirationCell SurvivalEnergy MetabolismGinsenosidesGlycolysisHeLa CellsHexokinaseHumansMembrane Potential, MitochondrialModels, BiologicalOxidative PhosphorylationReactive Oxygen SpeciesStress, PhysiologicalAdenosine Triphosphatebcl-2-Associated X Proteinginsenoside Rh2GinsenosidesHexokinaseReactive Oxygen SpeciesVoltage-Dependent Anion Channel 1

Identifiers

PMID33000213
PMCPMC7521551
OpenAlexW3085273061

What OpenQuestion 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 OpenQuestion graph.