Anticancer effects of baicalein on hepatocellular carcinoma cells.
Zheng, Yi-Hu ; Yin, Li-Hui ; Tan Grahn, Hooi Min LU
; Ye, Ai-Fang
; Zhao, Yan-Rong
and Zhang, Qi-Yu
(2014)
In Phytotherapy Research
28(9).
p.1342-1348
- Abstract
- The therapeutic potential of baicalein against hepatoma cells was evaluated in vitro and in vivo. In cell viability assays, baicalein showed significant cytotoxicity against the hepatocellular carcinoma cell lines H22, Bel-7404, and Hep G2 and moderate cytotoxicity against immortalized human hepatocytes. Baicalein induced G0/G1-phase arrest in hepatocellular carcinoma cells, inhibited AKT, and promoted the degradation of β-catenin and cyclin D1 without activation of GSK-3β. Furthermore, baicalein significantly inhibited H22 xenograft tumor growth without causing obvious adverse effects on weight or liver and spleen weight indexes in ICR mice. Immunohistochemical analysis showed that the inhibition of tumor growth in baicalein-treated mice... (More)
- The therapeutic potential of baicalein against hepatoma cells was evaluated in vitro and in vivo. In cell viability assays, baicalein showed significant cytotoxicity against the hepatocellular carcinoma cell lines H22, Bel-7404, and Hep G2 and moderate cytotoxicity against immortalized human hepatocytes. Baicalein induced G0/G1-phase arrest in hepatocellular carcinoma cells, inhibited AKT, and promoted the degradation of β-catenin and cyclin D1 without activation of GSK-3β. Furthermore, baicalein significantly inhibited H22 xenograft tumor growth without causing obvious adverse effects on weight or liver and spleen weight indexes in ICR mice. Immunohistochemical analysis showed that the inhibition of tumor growth in baicalein-treated mice was associated with decreased AKT, β-catenin, and cyclin D1 expression ex vivo. Our data indicate that baicalein might regulate cyclin D1 transcription via a β-catenin-dependent mechanism, leading to cell cycle arrest at G0/G1 phase and impaired cancer cell proliferation. These results suggest that baicalein is a potential candidate for the treatment of hepatocellular carcinoma. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/5425038
- author
- Zheng, Yi-Hu
; Yin, Li-Hui
; Tan Grahn, Hooi Min
LU
; Ye, Ai-Fang
; Zhao, Yan-Rong
and Zhang, Qi-Yu
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Glycogen Synthase Kinase 3: metabolism, Flavanones: pharmacology, Cyclin D1: metabolism, Cell Proliferation: drug effects, Cell Cycle Checkpoints: drug effects, Hepatocellular: metabolism, Hepatocellular: pathology, Carcinoma, Liver Neoplasms: metabolism, Liver Neoplasms: pathology, Proto-Oncogene Proteins c-akt: metabolism, beta Catenin: metabolism
- in
- Phytotherapy Research
- volume
- 28
- issue
- 9
- pages
- 1342 - 1348
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- pmid:24596136
- scopus:84907933131
- pmid:24596136
- ISSN
- 1099-1573
- DOI
- 10.1002/ptr.5135
- language
- English
- LU publication?
- no
- id
- caf7c72e-870c-4c3a-85d1-b965cf15f409 (old id 5425038)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/24596136?dopt=Abstract
- date added to LUP
- 2016-04-01 10:47:36
- date last changed
- 2022-03-12 17:06:25
@article{caf7c72e-870c-4c3a-85d1-b965cf15f409,
abstract = {{The therapeutic potential of baicalein against hepatoma cells was evaluated in vitro and in vivo. In cell viability assays, baicalein showed significant cytotoxicity against the hepatocellular carcinoma cell lines H22, Bel-7404, and Hep G2 and moderate cytotoxicity against immortalized human hepatocytes. Baicalein induced G0/G1-phase arrest in hepatocellular carcinoma cells, inhibited AKT, and promoted the degradation of β-catenin and cyclin D1 without activation of GSK-3β. Furthermore, baicalein significantly inhibited H22 xenograft tumor growth without causing obvious adverse effects on weight or liver and spleen weight indexes in ICR mice. Immunohistochemical analysis showed that the inhibition of tumor growth in baicalein-treated mice was associated with decreased AKT, β-catenin, and cyclin D1 expression ex vivo. Our data indicate that baicalein might regulate cyclin D1 transcription via a β-catenin-dependent mechanism, leading to cell cycle arrest at G0/G1 phase and impaired cancer cell proliferation. These results suggest that baicalein is a potential candidate for the treatment of hepatocellular carcinoma.}},
author = {{Zheng, Yi-Hu and Yin, Li-Hui and Tan Grahn, Hooi Min and Ye, Ai-Fang and Zhao, Yan-Rong and Zhang, Qi-Yu}},
issn = {{1099-1573}},
keywords = {{Glycogen Synthase Kinase 3: metabolism; Flavanones: pharmacology; Cyclin D1: metabolism; Cell Proliferation: drug effects; Cell Cycle Checkpoints: drug effects; Hepatocellular: metabolism; Hepatocellular: pathology; Carcinoma; Liver Neoplasms: metabolism; Liver Neoplasms: pathology; Proto-Oncogene Proteins c-akt: metabolism; beta Catenin: metabolism}},
language = {{eng}},
number = {{9}},
pages = {{1342--1348}},
publisher = {{John Wiley & Sons Inc.}},
series = {{Phytotherapy Research}},
title = {{Anticancer effects of baicalein on hepatocellular carcinoma cells.}},
url = {{http://dx.doi.org/10.1002/ptr.5135}},
doi = {{10.1002/ptr.5135}},
volume = {{28}},
year = {{2014}},
}