Proteome analysis of aflatoxin B₁-induced hepatocarcinogenesis in tree shrew (Tupaia belangeri chinensis) and functional identification of candidate protein peroxiredoxin II

• Published in: Proteomics (Weinheim) Vol. 8; no. 7; pp. 1490 - 1501
• Main Authors: Li, Yuan, Qin, Xue, Cui, Jiefeng, Dai, Zhi, Kang, Xiaonan, Yue, Haiying, Zhang, Yu, Su, Jianjia, Cao, Ji, Ou, Chao, Yang, Chun, Duan, Xiaoxian, Yue, Huifen, Liu, Yinkun
• Format: Journal Article
• Language: English
• Published: Weinheim Wiley-VCH Verlag 01.04.2008; WILEY-VCH Verlag; WILEY‐VCH Verlag; Wiley-VCH
• Subjects: Adult; Aflatoxin B1; Aged; Analytical, structural and metabolic biochemistry; Animals; Biological and medical sciences; Carcinoma; Carcinoma, Hepatocellular - chemically induced; Carcinoma, Hepatocellular - metabolism; Electrophoresis, Gel, Two-Dimensional; Female; Fundamental and applied biological sciences. Psychology; Gastroenterology. Liver. Pancreas. Abdomen; Hepatocellular; Humans; Liver Neoplasms - metabolism; Liver Neoplasms, Experimental - chemically induced; Liver Neoplasms, Experimental - metabolism; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Male; Mass Spectrometry; Medical sciences; Middle Aged; Miscellaneous; Peroxiredoxin II; Peroxiredoxins - biosynthesis; Peroxiredoxins - isolation & purification; Proteins; Reverse Transcriptase Polymerase Chain Reaction; Tree shrew; Tumors; Tupaia; Carcinoma; Hepatic disease; Proteome; Identification; Malignant tumor; Carcinogenesis; Peroxiredoxin II; Protein; Hepatocellular; Toxin; Liver cancer; Tree shrew; Proteomics; Aflatoxin B1; Digestive diseases; Cancer
• ISSN: 1615-9853; 1615-9861; 1615-9861
• DOI: 10.1002/pmic.200700229

In order to explore the proteins responsible for hepatocellular carcinoma (HCC), aflatoxin B₁-induced hepatocarcinogenesis in tree shrew (Tupaia belangeri chinensis) was analyzed with 2-DE and MS. By comparing HCC samples with their own precancerous biopsies and HCC-surrounding tissues, a group of candidate proteins that differentially expressed in HCC were obtained. Peroxiredoxin (Prx) II, one of the candidates with distinct alteration, was further investigated and validated. Western blot and RT-PCR assays confirmed the overexpression of Prx II in both tree shrew and human HCC tissues. RNA interference for silencing Prx II was employed subsequently to explore the function and underlying mechanism of Prx II on liver cancer cell line Hep3B. Results showed the cell proliferation and clone formation decreased obviously when Prx II expression was inhibited, while the flow cytometer analysis showed the percentage of cell apoptosis enhanced. Inhibition of Prx II expression also obviously increased the generation of ROS and malondialdehyde, both are the products from peroxidation. These results imply the important role of Prx II in hepatocarcinogenesis, possibly through its function in regulating peroxidation and hereby to provide a favorable microenvironment for cancer cell surviving and progressing.