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2‐D DIGE profiling of hepatocellular carcinoma tissues identified isoforms of far upstream binding protein (FUBP) as novel candidates in liver carcinogenesis
Author(s) -
Zubaidah Ramdzan M.,
Tan Gek San,
Tan Sandra B. E.,
Lim Seng Gee,
Lin Qingsong,
Chung Maxey C. M.
Publication year - 2008
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200800322
Subject(s) - hepatocellular carcinoma , gene isoform , carcinogenesis , proteomics , biology , cancer research , computational biology , biochemistry , gene
Hepatocellular carcinoma (HCC) is a major cause of cancer worldwide and is often characterized by aggressive tumour behaviour and poor prognosis. One of the major etiologies is hepatitis B or C virus (HBV or HCV) infections. In order to better comprehend the molecular mechanisms involved in HCC progression, we performed a systematic analysis on moderately and poorly differentiated human HCC tissues using 2‐D DIGE coupled to MALDI‐TOF/TOF MS. A total of 52 and 26 proteins were found to be dysregulated in moderately and poorly differentiated HCC tissues, respectively. For the first time, the over‐expression of a novel protein family, far upstream binding proteins (FUBPs) was identified in both stages of HCC and confirmed by western blots. FUBPs are of particular interest due to their transcriptional activity on the oncogene, c‐myc. It has generally been accepted that c‐myc plays an important role in HCC progression but its exact activators remain poorly understood. Interestingly, we also observed elevated c‐myc levels in the tissues used in this study by western blot analysis. We therefore propose that the FUBP family of proteins may be one of the possible upstream players that are involved in modulating the c‐myc levels in HCC tumorigenesis.