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Authors Zhu P, Liu Z, Zhou J, Chen Y
Received 31 August 2018
Accepted for publication 28 November 2018
Published 19 December 2018 Volume 2019:12 Pages 87—99
DOI https://doi.org/10.2147/OTT.S185997
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 2
Editor who approved publication: Dr Faris Farassati
Background: Tanshinol
is an active constituent of Salvia miltiorrhiza and possess
anti-inflammatory, antioxidant, and anti-bacterial activity. Herein, we
explored the role of tanshinol on the growth and aggressiveness of
hepatocellular carcinoma (HCC) cells in vitro and in vivo.
Materials and methods: The
proliferation of a panel of HCC cell lines was measured using MTT assay. The
expressions of phosphatidylinositol 3 kinase (PI3K) and protein kinase B (AKT)
were detected by immunofluorescence staining and immunohistochemical assay. The
levels of Bcl-2 and Bax were determined using immunoblotting assay. The
secretions of matrix metalloproteinase-2 (MMP-2) and MMP-9 were detected by
ELISA. The migration and invasion abilities of HepG2 cell were determined using
wound healing and Transwell invasion assays. The apoptosis of HepG2 cell
induced by tanshinol was analyzed by Annexin V/propidium iodide staining. A
xenograft model was constructed to investigate the inhibitory effect of
tanshinol on HepG2 cell growth in vivo. To further investigate the role of
tanshinol on the metastasis of HepG2 cell in vivo, an experimental metastasis
assay was performed.
Results: Tanshinol
inhibited the growth and colony formation of HCC cell in vitro. Tanshinol also
induced the apoptosis of HepG2 cell and inhibited the migration and invasion of
HepG2 cell. In in vivo experiments, tanshinol suppressed the tumor growth and
metastasis of HepG2 cell. Furthermore, the phosphorylation of PI3K and AKT was
decreased by tanshinol in vitro and in vivo.
Conclusion: Tanshinol
exerts its anti-cancer effects via regulating the PI3K-AKT signaling pathway in
HCC.
Keywords: tanshinol,
HCC, migration, invasion, apoptosis
