Abstract
Family with sequence similarity 189, member B (FAM189B), alias COTE1, a putative oncogene selected by microarray, for the first time was here found to be significantly up-regulated in hepatocellular carcinoma (HCC) specimens and HCC cell lines. mRNA expression of COTE1 in HCC samples and cell lines was detected by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR, while protein expression of COTE1 in HCC tissues was assessed by immunohistochemistry. In addition, invasion of HCC cells was observed after overexpressing or silencing COTE1. In the total of 48 paired HCC specimens, compared with the adjacent non-cancer tissues, the expression of COTE1 was up-regulated in 31 (p<0.01). In HCC cell lines, COTE1 expression was significantly higher than in normal human adult liver (p<0.01). Overexpression of COTE1 enhanced HCC-derived LM6 and MHCC-L cellular invasion in vitro. In contrast, COTE1 knockdown via RNAi markedly suppressed these phenotypes, as documented in LM3 and MHCC-H HCC cells. Mechanistic analyses indicated that COTE1 could physically associate with WW domain oxidoreductase (WWOX), a tumor suppressor. COTE1 may be closely correlated with invasion of hepatocellular carcinoma (HCC) cells and thus may serve as an effective target for gene therapy.
Highlights
Hepatocellular carcinoma (HCC) is one of the most fatal tumor worldwide, in Sub-Sahara Africa and South-eastern Asia (Parkin et al, 2005)
With sequence similarity 189, member B (FAM189B), alias COTE1, a putative oncogene selected by microarray, for the first time was here found to be significantly up-regulated in hepatocellular carcinoma (HCC) specimens and HCC cell lines. mRNA expression of COTE1 in HCC samples and cell lines was detected by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR, while protein expression of COTE1 in HCC tissues was assessed by immunohistochemistry
The results indicate that mRNA of COTE1 was obviously upregulated in HCC specimens (Figure 1A and B)
Summary
Hepatocellular carcinoma (HCC) is one of the most fatal tumor worldwide, in Sub-Sahara Africa and South-eastern Asia (Parkin et al, 2005). The protein has been identified as a potential binding partner of a WW domain-containing protein which is involved in tumor suppression (Ludes-Meyers et al, 2004; Abdeen et al, 2011). Hai Zhang et al wide approach, for the first time, we found COTE1 was markblely regulated in HCC clinical specimens, as compared to adjacent non-cancerous livers (data not shown). We verified upregulation of COTE1 in 31 of 48 paired HCC specimens and 4 invasive HCC cell lines. These indicated it may contribute to cellular invasion of HCC as a new potential oncogene. The mechanistic analyses indicated that COTE1 could physically interact with WW domain oxidoreductase (WWOX), a tumor suppressor
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