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Silibinin suppresses bladder cancer through down-regulation of actin cytoskeleton and PI3K/Akt signaling pathways

  • Mitsuho Imai-Sumida
    ,
  • Takeshi Chiyomaru
    ,
  • Shahana Majid
    ,
  • ,
  • Hannah Nip
    ,
  • Rajvir Dahiya
*Corresponding author for this work
  • VA Medical Center
    ,
  • National Hospital Organization Kagoshima Medical Center
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Silibinin is the major active constituent of silymarin, an extract of milk thistle seeds. Silibinin has been shown to have significant anti-cancer effects in a variety of malignancies. However, the molecular mechanisms of silibinin action in bladder cancer have not been studied extensively. In the present study, we found that silibinin (10 μM) significantly suppressed proliferation, migration, invasion and induced apoptosis of T24 and UM-UC-3 human bladder cancer cells. Silibinin down-regulated the actin cytoskeleton and phosphatidylinositide 3-kinase (PI3K)/Akt signaling pathways in these cancer cell lines. These pathways were found to crosstalk through RAS cascades. We found that silibinin suppressed levels of trimethylated histone H3 lysine 4 and acetylated H3 at the KRAS promoter. Furthermore, silibinin targets long non-coding RNA: HOTAIR and ZFAS1, which are known to play roles as oncogenic factors in various cancers. This study shows that silibinin exerts anti-cancer effects through down-regulation of actin cytoskeleton and PI3K/Akt pathways and thus suppresses bladder cancer growth and progression.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 92032-92042 (11 pages)

Journal (Volume, Issue Number)

Oncotarget (Volume 8, Issue 54)

Publication milestones

  • Published - 2017

Publication status

Published - 2017

ISSN

1949-2553

Publication IDs

  • Scopus: 85032686077
  • PubMed: 29190895

Publication metrics

Metrics

SciVal
FWCI
1.26
SciVal
Author count
8
SciVal
citations
19
SciVal
Paper percentile
87
Fractional count
1
Fractional count
0.13
Fractional count
7
Fractional count
0.88
Fractional count
1
Fractional count
1
Scopus
citations

PlumX, opens in new tab

Citation count
51
Captures
34

Funding Details

Mitsuho Imai-Sumida was supported by the Astellas Foundation for Research on Metabolic Disorders fellowship funded by Astellas Pharma, Inc. This work was supported by National Institutes of Health Grant R01CA196848, RO1CA138642, RO1CA160079, RO1CA199694 and RO1CA184966. This study was also supported by Veterans Affairs Program Project BX001604 and Veterans Affairs Merit Review grants.