Project description:A comparative microarray analysis of indolent or aggressive mouse oral cancer cell lines was performed to identify gene expression signatures and specific molecules involved in aggressive tumor growth.
Project description:PURPOSE: To provide a detailed gene expression profile of the normal postnatal mouse cornea. METHODS: Serial analysis of gene expression (SAGE) was performed on postnatal day (PN)9 and adult mouse (6 week) total corneas. The expression of selected genes was analyzed by in situ hybridization. RESULTS: A total of 64,272 PN9 and 62,206 adult tags were sequenced. Mouse corneal transcriptomes are composed of at least 19,544 and 18,509 unique mRNAs, respectively. One third of the unique tags were expressed at both stages, whereas a third was identified exclusively in PN9 or adult corneas. Three hundred thirty-four PN9 and 339 adult tags were enriched more than fivefold over other published nonocular libraries. Abundant transcripts were associated with metabolic functions, redox activities, and barrier integrity. Three members of the Ly-6/uPAR family whose functions are unknown in the cornea constitute more than 1% of the total mRNA. Aquaporin 5, epithelial membrane protein and glutathione-S-transferase (GST) omega-1, and GST alpha-4 mRNAs were preferentially expressed in distinct corneal epithelial layers, providing new markers for stratification. More than 200 tags were differentially expressed, of which 25 mediate transcription. CONCLUSIONS: In addition to providing a detailed profile of expressed genes in the PN9 and mature mouse cornea, the present SAGE data demonstrate dynamic changes in gene expression after eye opening and provide new probes for exploring corneal epithelial cell stratification, development, and function and for exploring the intricate relationship between programmed and environmentally induced gene expression in the cornea. Keywords: other
Project description:A comparative microarray analysis of indolent or aggressive mouse oral cancer cell lines was performed to identify gene expression signatures and specific molecules involved in aggressive tumor growth. We compared 3 indolent cell lines (MOC1, MOC22, MOC23) to 1 aggressive line and it's derivatives (MOC2, MOC2-7 and MOC2-10). We also included a cell line generated from a lymph node metastasis of the MOC2 tumor. The lines were all analyzed in triplicated except for MOC1 which was done in quadruplicate. Finally, we included duplicate samples of primary, normal C57BL/6 oral keratinocytes grown in the same media as the MOC cell lines.
