OBJECTIVETo investigate the complex differences between high metastatic and low metastatic cells of the Adenoid cystic Carcinoma.

METHODSGene expression patterns were examined in high metastatic cell ACC-M strain and low metastatic ACC-2 strain with the method SSH (suppression subtractive hybridization).

RESULTSalthough extensive similarity was noted between the expression profiles, twelve genes were highly expressed of, in low metastatic cell ACC-2 tester, compared with driver, high metastatic cell ACC-M. These genes were cysteine-rich angiogenic-inducer protein (cyr61), chromosome7 clone RP11-52501, G protein, was family member Iferritin heavy polypeptide I, jumping translocation breakpoint, eukaryotic translation elongation, folate receptor, ribosomal proteins L7a, S21, P0 and other two novel genes-ACC metastasis-associated RNH and ACC metastasis-associated suspected protein. GenBank accession number were AF522024 and AF522025 respectively.

CONCLUSIONSthe result suggests that the obtainment of the ability of metastasis is related to the low expression or mutation of these genes. These data provide insight into the extent of expression differences underlying metastasis-related genes that may prove useful as diagnostic or prognostic markers.

Base Sequence ; Blotting, Northern ; Carcinoma, Adenoid Cystic ; genetics ; secondary ; Cell Line, Tumor ; Gene Expression Profiling ; Humans ; Molecular Sequence Data ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo form ACC-M-GFP cells by transfecting pEGFP-1 into ACC-M cells, and to build up lung metastasis model of adenoid cystic carcinoma for dynamic observation in simulated lung environment.

METHODSpEGFP-1 was prepared and then transfected into ACC-M cell lines by using cationic lipid-based gene transfer technique. After successive selection, the ACC-M-GFP cells were collected and inoculated in BALB/C mice. The simulated lung environment was built up, and dynamic observation was performed by laser confocal microscopy within four weeks after transfection.

RESULTSThe amount of fluorescent tumor cell colonies and the intensity of fluorescence gradually increased from the second week to the forth week after transfection. In the meantime, only a very small number of tumor cells had the ability to form clones.

CONCLUSIONSWe successfully built up a lung metastasis model of adenoid cystic carcinoma for dynamic observation. The model is suitable for capturing and analyzing metastatic tumor cells in early stage.

Animals ; Carcinoma, Adenoid Cystic ; secondary ; Cell Line, Tumor ; Green Fluorescent Proteins ; genetics ; Humans ; Lung Neoplasms ; secondary ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mouth Neoplasms ; pathology ; Neoplasm Metastasis ; Neoplasms, Experimental ; Transfection

We searched for metastasis-related genes in adenoid cystic carcinoma by suppression subtractive hybridization analysis of high and low metastasis cell lines. Twelve genes (ten previously identified and two novel sequences) were identified as being expressed at lower levels in high metastasis cell line Acc-M when compared to low metastasis cell line Acc-2. The known sequences corresponded to the genes for cysteine-rich angiogenesis induction factor (cyr61), chromosome 7 RP11-52501 clone, G-protein, WAS familial ferritin I heavy chain, jumping translocation breakpoint, eukaryotic translation elongation, folate receptor and three ribosomal proteins. Among them, the G protein and ferritin I heavy chain genes contained mutations in the high metastasis cell line. The two novel gene sequences have been named ACC metastasis-associated RNH and ACC metastasis-associated suspected protein (GenBank # AF522024 and AF522025, respectively). Taken together, these results suggest that reduced expression and/or mutation of several genes in the tumor cell line Acc-M are associated with high tumor metastasis, providing important molecular biological materials for further study of metastasis control and possible targets for cancer gene therapy.
Blotting, Northern ; Carcinoma, Adenoid Cystic/*genetics/secondary ; *Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Human ; In Vitro ; Molecular Sequence Data ; Neoplasm Metastasis/*genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Cells, Cultured