VSIG4 is overexpressed in ovarian cancers compared with that in benign tumors. This finding supports VSIG4 being used as a potential therapeutic target for ovarian cancer. Furthermore, soluble VSIG4 levels are associated with the progression and recurrence of ovarian cancer, indicating that soluble VSIG4 may be used as a potential biomarker for predicting tumor prognosis.

Promoter hypermethylation of the ADAM23 gene, which is normally involved in cell-to-cell and cell-to matrix adhesion, has been reported in pancreatic, breast and brain cancer, and recently the role of this gene was examined in gastric cancer. In this study, we analyzed ADAM23 expression in colorectal cancer cell lines and examined its methylation by methylation-specific PCR (MSP) and bisulfate-modified DNA sequencing analysis. Methylated cells were treated with 5-aza-2 0 -deoxycytidine to restore the ADAM23 expression. We then examined ADAM23 methylation status in colorectal cancer tissues and their corresponding normal tissues. We found that ADAM23 was aberrantly silenced or expressed at very low levels in 28 of the 32 (88%) colorectal cancer cell lines. MSP analysis showed that ADAM23 was methylated in 29 of 32 (91%) colorectal cancer cell lines and attenuated expression of ADAM23 was found to be related to hypermethylation in its promoter region. Moreover, the CpG dinucleotide methylation threshold of 70-90% was found to be required for complete silencing. In addition, when some cell lines without ADAM23 expression were treated with 5-aza-2 0 -deoxycytidine, ADAM23 was reexpressed. In colorectal cancer tissues, the promoter region of ADAM23 was hypermethylated in 36 of 76 (47%). These results demonstrated that ADAM23 may be down-regulated by aberrant promoter hypermethylation during the progression of colorectal cancer. ' 2008 Wiley-Liss, Inc.Key words: ADAM23 gene; methylation; methylation-specific PCR (MSP); colorectal cancer; cancer cell lines Colorectal cancer is the third most common cancer in both males and females in the United States, although incidence rates have decreased from 1998 through 2004. 1 In Korea, colorectal cancer is the fourth common cancer in both sexes. 2 Moreover, evidence indicates that most cancers have a genetic component. 3 However, it is also believed that epigenetic mechanisms may also have a significant role in colorectal cancer development, 4 and methylation of the C 5 position of cytosine residues in DNA is one of the most fundamental epigenetic characteristics. This methylation is performed by DNA methyltransferases (DNMTs), which have been implicated in many processes including transcriptional regulation, genomic stability, X-chromosome inactivation and in the silencing of parasitic DNA transposable elements. 5 In a recent study, it was estimated that up to 80% of all CpG dinucleotides in the genome are methylated. 6 Furthermore, unmethylated CpG residues are known to be predominantly located in the promoter regions of active and inducible genes. They are referred to as CpG islands, 7 which consist of regions of more than 500 base pairs with the GC content exceeding 55%. 6 The importance of DNA methylation was highlighted by the finding that many human disease result from abnormal control. 8 Moreover, the aberrant methylation of CpG islands is a characteristic of many human cancers and may be found during early carcinogenesis. 9 This methylation may silence many genes, esp...

DNA methylation patterns in CpG-rich regions of promoter, CpG islands, are concerned in regulation of gene expression in mammalian cells. Excessive methylation of CpG dinucleotides in promoter represses the gene expression. In cancer, especially, gene silencing is occurred through aberrant methylation in promoter of tumor suppressor genes. Methylation-specific PCR (MSP) is a method for analysis of DNA methylation patterns in CpG islands. For performing MSP, DNA is modified by and PCR performed with two primer pairs, which are detectable methylated and unmethylated DNA, respectively. MSP is a rapid measure for assession of the methylation status in CpG island.

Transcriptional repression of CD133 is caused by promoter hypermethylation of the CD133 CpG islands in some of colorectal cancer cell lines. The study may contribute to the understanding of the role of CD133 inactivation in the progression of colorectal cancers.

Permanently growing cell lines can be invaluable because of their usefulness in a variety of experimental situations. We report the characteristics of seven cell lines designated, SNU-306, SNU-334, SNU-1528, SNU-1553, SNU-1581, SNU-1958 and SNU-2372, which were established from three primary carcinomas, two pleural effusion, one pericardial effusion and one ascitic fluid samples obtained from seven Korean breast carcinoma patients. The histopathology of the primary tumors and their in vitro growth characteristics are described. DNA fingerprinting analysis and genetic alterations in the p53 and EGFR genes were conducted. The expression levels of the ER-α, PR, C-erbB2, E-cadherin, COX-2, MDR and MXR genes were investigated and sensitivity to anticancer drugs was screened. Growth was as adherent cells (four cell lines), floating aggregates (one cell line) and both (two cell lines). All lines were free of mycoplasma or bacteria and were proven unique by DNA fingerprinting analysis using 18 microsatellite markers. Estrogen receptor (ER) mRNA was highly expressed in five cell lines and low or undetectable in SNU-1958 and SNU-2372. Progesterone receptor (PR) mRNA was expressed only in the SNU-306. SNU-1958 and SNU-2372 were hormone receptor-negative and C-erbB2-negative (triple-negative). SNU-1528 had an in-frame deletion of 42 base pairs of p53 gene and showed over 20-fold resistance for taxol compared to the other cell lines. There were no mutation in the EGFR gene; COX-2 was expressed in four cell lines and MXR was expressed in two cell lines. These well-characterized seven breast cancer cell lines, which include two triple-negative cell lines, will be useful for the study of breast cancer biology.