Effects of tetrazanbigen on the protein expression in human hepatocellular carcinoma cell line QGY-7701.
- Author:
Yonghua, YUAN
;
Wei, LI
;
Longjiang, LI
;
Xiaolan, YANG
;
Rong, GU
;
Huabo, LIU
;
Kaishun, HUANG
;
Yu, YU
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents/*pharmacology;
Azo Compounds/*pharmacology;
Carcinoma, Hepatocellular/*pathology;
Cell Line, Tumor;
Gonanes/*pharmacology;
Liver Neoplasms/*pathology;
Proteins/*metabolism;
Proteome
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2009;29(3):304-8
- CountryChina
- Language:English
-
Abstract:
Tetrazanbigen (TNBG) is a novel synthetic antitumor drug with significant antitumor effects on common solid tumors in vitro and in vivo. It may lead to death of cancer cells through a tumor-associated lipoidosis mechanism, and result in lipid droplets (LDs) accumulation at the cytoplasm. In this study, the effects of TNBG on protein expression in human hepatocellular carcinoma cell line QGY-7701 were studied for elucidating its antitumor mechanism. The proteins extracted from TNBG-treated human hepatocellular carcinoma cell line QGY-7701 were analyzed and compared with control cells by two-dimensional gel electrophoresis. The differential proteins were identified by matrix-associated laser desorption ionization time-of-flight mass (MALDI-TOF-MS) spectrometry. Two proteins of interest, the levels of which were significantly increased in TNBG-treated cells, were further characterized by Western blot analysis. The results showed a total of 846+/-23 spots in control cells and 853+/-30 spots in TNBG-treated cells. Twenty-six up-regulated or down-regulated proteins were found by analyzing differential proteomic 2-DE map. Eleven of them were identified by mass spectrometry. They were protein disulfide-isomerase precursor, 94 kD glucose-regulated protein, heat shock protein (HSP) 90-alpha, ATP-citrate lyase, HMG-CoA reductase, glucose-6-phosphate 1-dehydrogenase, very-long-chain specific acyl-CoA dehydrogenase, squalene synthetase, sterol regulatory element-binding protein 1, fructose-bisphosphate aldolase A, and peroxiredoxin-1. These up-regulated or down-regulated proteins are mostly related to lipid metabolism. The TNBG antitumor mechanism is probably to influence tumor lipid metabolism, resulting in accumulation of LDs in tumor cells.
