Evidence map›Paper›PMID 27825116›Full record

ArticleOncotarget2017

Ginsenoside-Rb1 targets chemotherapy-resistant ovarian cancer stem cells via simultaneous inhibition of Wnt/β-catenin signaling and epithelial-to-mesenchymal transition.

Shan Deng, Chris Kong Chu Wong, Hung-Cheng Lai, Alice Sze Tsai Wong

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 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
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  8. Nutrients · 2024
    Review
  9. Review
  10. Review
  11. Review
  12. Targeting ovarian cancer stem cells: a new way out.Stem cell research & therapy · 2023
    Review
  13. Article
  14. Ginsenosides on stem cells fate specification-a novel perspective.Frontiers in cell and developmental biology · 2023
    Review
  15. Review
  16. Review
  17. Review
  18. A spotlight on underlying the mechanism of AMPK in diabetes complications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
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  20. Review
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

4 authors at 3 institutions in 2 countries.

Shan DengSchool of Biological Sciences, University of Hong Kong, Hong Kong.
Chris Kong Chu WongDepartment of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong.
Hung-Cheng LaiDepartment of Obstetrics and Gynecology, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.
Alice Sze Tsai WongSchool of Biological Sciences, University of Hong Kong, Hong Kong.
Hong Kong Baptist University · HKTaipei Medical University-Shuang Ho Hospital · TWUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance is a major clinical problem compromising the successful treatment of cancer. One exciting approach is the eradication of cancer stem/tumor-initiating cells (jointly CSCs), which account for tumor initiation, progression, and drug resistance. Here we show for the first time, with mechanism-based evidence, that ginsenoside-Rb1, a natural saponin isolated from the rhizome of Panax quinquefolius and notoginseng, exhibits potent cytotoxicity on CSCs. Rb1 and its metabolite compound K could effectively suppress CSC self-renewal without regrowth. Rb1 and compound K treatment also sensitized the CSCs to clinically relevant doses of cisplatin and paclitaxel. These effects were associated with the Wnt/β-catenin signaling pathway by downregulating β-catenin/T-cell factor-dependent transcription and expression of its target genes ATP-binding cassette G2 and P-glycoprotein. We also identified reversal of epithelial-to-mesenchymal transition as a new player in the Rb1 and compound K-mediated inhibition of CSCs. Rb1 and compound K treatment also inhibited the self-renewal of CSCs derived from ovarian carcinoma patients as well as in xenograft tumor model. Moreover, we did not observe toxicity in response to doses of Rb1 and compound K that produced an anti-CSC effect. Therefore, Rb1 should be explored further as a promising nutraceutical prototype of treating refractory tumors.

Indexed as

Drug Resistance, NeoplasmAnimalsCell Line, TumorCell ProliferationCell Self RenewalDisease Models, AnimalEpithelial-Mesenchymal TransitionFemaleGinsenosidesHumansMiceMitogen-Activated Protein KinasesNeoplastic Stem CellsOvarian NeoplasmsProto-Oncogene Proteins c-aktSignal Transductionginsenoside compound Kginsenoside Rb1GinsenosidesMitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktcancer stem cellschemoresistanceginsenosideovarian cancerWnt/β-catenin signaling

Identifiers

PMID27825116
PMCPMC5432225
OpenAlexW2546707314

What OpenQuestion holds

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Registered trials

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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.