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BioMed Research International
Volume 2013 (2013), Article ID 317926, 7 pages
Research Article

Profiling of Hepatocellular Carcinoma Cell Cycle Regulating Genes Targeted by Calycosin

1Department of Blood Transfusion, General Hospital of PLA, Beijing 100853, China
2Department of Toxicology, Beijing Center for Diseases Control and Prevention, Beijing 100013, China

Received 30 July 2013; Revised 18 October 2013; Accepted 2 December 2013

Academic Editor: Wei Mike Liu

Copyright © 2013 Dongqing Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We cocultured calycosin with human hepatocellular carcinoma cell line (BEL-7402) to investigate the effect on cell proliferation. Calycosin can markedly block the cell growth in G1 phase ( ) on the IC50 concentration. There were seventeen genes involved in cell-cycle regulation showing differentially expressed in treated cells detected by gene chip. Eight genes were upregulated and nine genes were downregulated. Downregulated TFDP-1, CDKN2D, and SPK2 and upregulated CDC2 and CCNB1 might affect cell cycle of tumor cells. Furthermore, we checked the transcription pattern using 2D gel method to find different expression of proteins in human hepatocellular carcinoma cells after exposure to calycosin. Fourteen proteins were identified by matrix-assisted laser desorption/ionization-time of flight-mass spectrometry (MALDI-TOF-MS). Twelve proteins expression were increased such as transgelin 2, pyridoxine 5′-phosphate, stress-induced-phosphoprotein 1, peroxiredoxin 1, endoplasmic reticulum protein 29, and phosphoglycerate mutase 1. Only thioredoxin peroxidase and high-mobility group box1 proteins’ expression decreased. Both genes and proteins changes might be relate to the mechanism of antitumor effect under treatment of calycosin. In conclusion, calycosin has a potential effect to inhibit the BEL-7402 cell growth by inhibiting some oncogene expression and increasing anticancer genes expression, what is more, by blocking cell cycle.