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Gene expression analyses of mir-31 overexpression in ovarian serous cancer cell line

ABSTRACT: A variety of human cancers demonstrate alterations in microRNA expression. We hypothesized that regulatory defects in microRNAs play a central early role in organizing the molecular changes involved in ovarian cancer (OvCa). Using both gene arrays and deep sequencing, we comprehensively profiled mRNA and microRNA expression, respectively, in human serous epithelial OvCa cell lines, serous tumors, and short-term primary cultures of normal ovarian surface epithelium (NOSE). We expected that over-expression of a specific microRNA would lead to lower expression of its mRNA targets, and under-expression of a specific microRNA would lead to higher expression of its target genes. Using our expression data in conjunction with established in silico algorithms, we found putative microRNA:mRNA functional pairs. Furthermore, gene expression profiles were taken of serous cultures having functional knockdown or over-expression of specific microRNAs of interest. Over-expression of mir-31 (found under-expressed in serous OvCa) resulted in down-regulation in vitro of a significant number of the in silico predicted mir-31 target genes. Keywords: two group comparison

ORGANISM(S): Homo sapiens

PROVIDER: GSE16700 | GEO | 2010/02/25

SECONDARY ACCESSION(S): PRJNA122799

REPOSITORIES: GEO

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Project description:Background. Genome-wide expression changes are associated with development of chemoresistance in patients with ovarian cancer (OVCA); the BCL2 antagonist of cell death (BAD) apoptosis pathway may play a role in clinical outcome. Methods. We analyzed specimens and/or genomic data from 1,406 patients and 116 cancer cell lines. Genome-wide expression changes and cisplatin-resistance were evaluated in OVCA cell lines subjected to a total of 144 (cisplatin)-treatment/recovery cycles. Pathway analysis was performed on genes associated with increasing cisplatin-resistance. BAD protein phosphorylation was studied in patient samples and cell lines, and small interfering RNAs (siRNA) used to explore the pathway as a therapeutic target. We evaluated the influence of BAD-pathway expression on chemosensitivity and/or clinical outcome using genomic data from 60 human cancer cell lines and ovarian, breast, colon, and brain cancers from 1,258 patients. Results. The BAD pathway was associated with evolution of OVCA cell line cisplatin-resistance (P<0.001) and resistance of 7 human cancer cell types to 8 cytotoxic agents (P<0.05). OVCA chemoresistance was associated with BAD protein phosphorylation, and targeted siRNA modulation produced corresponding changes in chemosensitivity. Expression of a 47-gene BAD-pathway signature was associated with survival of 1,258 patients with ovarian, breast, colon, and brain cancer. The OVCA BAD-pathway signature survival advantage was independent of surgical cytoreductive status. Conclusions. The BAD apoptosis pathway influences the sensitivity of human cancers to a variety of chemotherapies, likely via modulation of BAD-phosphorylation. The pathway has clinical relevance as a potential biomarker of therapeutic response, patient survival, and as a promising therapeutic target. Twenty-eight (28) advanced-stage serous epithelial ovarian cancers were resected at the time of primary surgery from patients who would receive platinum-based therapy. The tumors were arrayed on Affymetrix HG-U133A GeneChips. The samples were analyzed with respect to the BAD pathway for correlation to overall survival and cisplatin response.

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Gene expression analyses of mir-31 overexpression in ovarian serous cancer cell line

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