Abstract 4171: Tumor suppressive microRNA-218 mediated focal adhesion pathways in cervical squamous cell carcinoma
Background: MicroRNAs (miRNAs), a class of small non-coding RNAs, regulate protein-coding gene expression by repressing translation or cleaving RNA transcripts in a sequence-specific manner. A growing body of evidence suggests that miRNAs contribute to cervical squamous cell carcinoma (cervical-SCC)...
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Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2013-04, Vol.73 (8_Supplement), p.4171-4171 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Background:
MicroRNAs (miRNAs), a class of small non-coding RNAs, regulate protein-coding gene expression by repressing translation or cleaving RNA transcripts in a sequence-specific manner. A growing body of evidence suggests that miRNAs contribute to cervical squamous cell carcinoma (cervical-SCC) progression, development, and metastasis. Recent our miRNA expression signature of SCC (hypopharyngeal-SCC and esophageal-SCC) revealed that microRNA-218 (miR-218) was significantly reduced in cancer tissues. The study of the aim was to investigate the functional significance of miR-218 and its mediated molecular pathways in cervical-SCC.
Methods:
Gain-of-function studies were performed to investigate cancer cell proliferation, migration and invasion by restoration of mature miRNAs into HPV positive or negative cervical-SCC cell lines (CaSKi, HeLa, ME180 and YUMOTO). To identify the biological processes or pathways potentially regulated by the miRNAs, we applied genome-wide gene expression analysis and in silico study. The GENECODIS software assigned a number of the putative miRNA targets to known pathways in KEGG [http://www.genome.jp/kegg/pathway.html]. Gene expression analyses of all candidate genes involved in each of the pathways using GEO (http://www.ncbi.nlm.nih.gov/geo/) database.
Results:
Expression levels of miR-218 were significantly reduced in cervical-SCC clinical specimens compared to adjacent non-cancerous tissues (P |
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ISSN: | 0008-5472 1538-7445 |
DOI: | 10.1158/1538-7445.AM2013-4171 |