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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)
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author
publishing date
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Contribution to journal
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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
external identifiers
  • pmid:24596136
  • scopus:84907933131
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
2015-05-21 07:41:30
date last changed
2017-10-29 03:16:37
@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},
  keyword      = {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},
  series       = {Phytotherapy Research},
  title        = {Anticancer effects of baicalein on hepatocellular carcinoma cells.},
  url          = {http://dx.doi.org/10.1002/ptr.5135},
  volume       = {28},
  year         = {2014},
}