Establishment and characterization of seven human breast cancer cell lines including two triple-negative cell lines.

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.

Protective role of V-set and immunoglobulin domain-containing 4 expressed on kupffer cells during immune-mediated liver injury by inducing tolerance of liver T- and natural killer T-cells.

Unlabelled: V-set and Ig domain-containing 4 (VSIG4, CRIg, or Z39Ig), a newly identified B7-related cosignaling molecule, is a complement receptor and a coinhibitory ligand that negatively regulates T-cell immunity. Despite its exclusive expression on liver Kupffer cells (KCs) that play key roles in liver tolerance, the physiological role of VSIG4 in liver tolerance remains undefined. Mice lacking VSIG4 had poor survival rates and severe liver pathology in a concanavalin A (ConA)-induced hepatitis (CIH) model, which could be prevented by adoptive transfer of VSIG4(+) KCs.

Methylation-specific PCR.

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.

Establishment and characterization of six human lung cancer cell lines: EGFR, p53 gene mutations and expressions of drug sensitivity genes.

Background: Six human lung cancer cell lines (SNU-371, SNU-963, SNU-1327, SNU-1330, SNU-2292 and SNU-2315) were newly established through primary cell cultures. These cell lines were derived from a pulmonary blastoma, a small cell lung cancer, three adenocarcinomas and a squamous cell carcinoma of the lung of six Korean lung cancer patients.

Methods: The histopathology of the primary tumors and their in vitro growth characteristics were described.

Promoter hypermethylation and loss of CD133 gene expression in colorectal cancers.

Aim: To understand CD133 promoter hypermethylation and expression in 32 colorectal cancer cell lines.

Methods: Nucleic acid was isolated from 32 colorectal cancer cell lines and CD133 expression levels were measured by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR. Promoter methylation status of the CD133 gene was analyzed with a methylation-specific PCR after sodium-bisulfite modification and by clonal sequencing analysis.

Establishment and characterization of 13 human colorectal carcinoma cell lines: mutations of genes and expressions of drug-sensitivity genes and cancer stem cell markers.

Thirteen human colorectal cancer (CRC) cell lines were established from 10 primary tumors and 3 metastatic tumors obtained from 13 Korean patients. Characteristics of the cell lines including morphology in vivo and in vitro; mutations of the K-ras, p53, APC and MMR genes and microsatellite instability (MSI) status in vitro were determined. Expression of drug-sensitivity genes including MDR1, MXR, MRP1 and COX2 was also analyzed.

Promoter hypermethylation of the ADAM23 gene in colorectal cancer cell lines and cancer tissues.

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'-deoxycytidine to restore the ADAM23 expression.