Evidence map›Paper›PMID 29528145›Full record

ArticleMolecular carcinogenesis2018

Timosaponin A-III inhibits oncogenic phenotype via regulation of PcG protein BMI1 in breast cancer cells.

Joseph E Gergely, Armond E Dorsey, Goberdhan P Dimri, Manjari Dimri

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  7. Targeting miRNA by Natural Products: A Novel Therapeutic Approach for Nonalcoholic Fatty Liver.Evidence-based complementary and alternative medicine : eCAM · 2021
    Review
  8. Molecular principles of metastasis: a hallmark of cancer revisited.Signal transduction and targeted therapy · 2020
    Review
  9. Review
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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

4 authors at 1 institution in 1 country.

Joseph E GergelyDepartment of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, District of Columbia.
Armond E DorseyDepartment of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, District of Columbia.
Goberdhan P DimriDepartment of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, District of Columbia.ORCID 0000-0003-0280-1242
Manjari DimriDepartment of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, District of Columbia.
George Washington University · US

Funding

The role of BMI1 in breast cancerR01CA094150 · NCI · NORTHSHORE UNIV HEALTHSYSTEM RES INST · PI DIMRI, GOBERDHAN P · 2003 to 2013
$2.7M
A novel regulator of triple negative breast cancer and breast cancer stem cell phenotypeR03CA223946 · NCI · GEORGE WASHINGTON UNIVERSITY · PI DIMRI, MANJARI · 2018 to 2019
$160k
A chemopreventive approach of targeting breast cancer stem cellsR03CA198614 · NCI · GEORGE WASHINGTON UNIVERSITY · PI DIMRI, MANJARI · 2015 to 2016
$159k
NCI NIH HHS R01 CA094150NCI NIH HHS R03 CA198614NCI NIH HHS R03 CA223946
6 · The paper itself

Abstract

Polycomb group (PcG) protein BMI1 is an important regulator of oncogenic phenotype and is often overexpressed in several human malignancies including breast cancer. Aberrant expression of BMI1 is associated with metastasis and poor prognosis in cancer patients. At present, therapy reagents that can efficiently inhibit the expression of BMI1 are not very well known. Here, we report that Timosaponin A-III (TA-III), a steroidal saponin obtained from the rhizomes of an herb, Anemarrhena asphodeloides, strongly inhibits expression of BMI1 in breast cancer cells. Treatment of breast cancer cells with TA-III resulted in inhibition of oncogenic phenotypes such as proliferation, migration and invasion, and induction of cellular senescence. Inhibition of these oncogenic phenotypes was accompanied by downregulation of BMI1 expression and histone posttranslational modification activity of PRC1. The mechanistic analysis of TA-III-induced inhibition of oncogenic activity and BMI1 expression suggests that downregulation of c-Myc mediates TA-III effect on BMI1. We further show that exogenous BMI1 overexpression can overcome TA-III-induced inhibition of oncogenic phenotypes. We also show that TA-III induces expression of tumor suppressive miR-200c and miR-141, which are negatively regulated by BMI1. In summary, our data suggest that TA-III is a potent inhibitor of BMI1 and that it can be successfully used to inhibit the growth of tumors where PcG protein BMI1 and PcG activities are upregulated.

Indexed as

Breast NeoplasmsCarcinogenesisCell Line, TumorCell MovementCell ProliferationCellular SenescenceDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMicroRNAsOncogenesPhenotypePolycomb-Group ProteinsPolycomb Repressive Complex 1BMI1 protein, humanMicroRNAsPolycomb-Group ProteinsPolycomb Repressive Complex 1SaponinsSteroidstimosaponin AIIIBMI1breast cancercellular senescencemiR-141miR-200cpolycomb group proteinsTimosaponin A-IIItumor suppressors

Identifiers

PMID29528145
PMCPMC5986597
OpenAlexW2789488081

What OpenQuestion holds

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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.