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Resistance of primary ovarian cancer cells to oncolytic adenoviruses

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE15473 | GEO | 2009/04/01

SECONDARY ACCESSION(S): PRJNA115915

REPOSITORIES: GEO

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Resistance of primary ovarian cancer cells to oncolytic adenoviruses

Project description:This SuperSeries is composed of the following subset Series: GSE15350: Resistance of primary ovarian cancer cells to oncolytic adenoviruses part1 of 2 GSE15351: Resistance of primary ovarian cancer cells to oncolytic adenoviruses part2 of 2 Refer to individual Series

2009-04-01 | E-GEOD-15473 | biostudies-arrayexpress

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Project description:The mechanisms of primary ovarian cancer cells for resistance to viral oncolysis were investigated using Ad5/35.IR.E1A/TRAIL on clonal cultures derived from ovc316m cells. Part 1 of 2, initital study involving 5 clonal ovc316m cultures Cells were infected for 8 days and cell survival determined by MTT assay. Uninfected control cells of each clonal culture were utilized for DNA expression arrays. SKOV3-ip1 cells were used for reference RNA in all samples.

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Resistance of primary ovarian cancer cells to oncolytic adenoviruses part2 of 2

Project description:The mechanisms of primary ovarian cancer cells for resistance to viral oncolysis were investigated using Ad5/35.IR.E1A/TRAIL on clonal cultures derived from ovc316m cells. Part 2 of 2, 26 clonal ovc316m cultures additionally to Resistance of primary ovarian cancer cells to oncolytic adenoviruses part1 of 2 Cells were infected for 8 days and cell survival determined by MTT assay. Uninfected control cells of each clonal culture were utilized for DNA expression arrays. SKOV3-ip1 cells were used for reference RNA in all samples. The reference RNA from SKOV3-ip1 cells for part 2 of 2 had to be re-amplified.

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Epithelial phenotype confers resistance of ovarian cancer cells to oncolytic adenoviruses.

Project description:We studied the susceptibility of primary ovarian cancer cells to oncolytic adenoviruses. Using gene expression profiling of cancer cells either resistant or susceptible to viral oncolysis, we discovered that the epithelial phenotype of ovarian cancer represents a barrier to infection by commonly used oncolytic adenoviruses targeted to coxsackie-adenovirus receptor or CD46. Specifically, we found that these adenovirus receptors were trapped in tight junctions and not accessible for virus binding. Accessibility to viral receptors was critically linked to depolarization and the loss of tight and adherens junctions, both hallmarks of epithelial-to-mesenchymal transition (EMT). We showed that specific, thus far little-explored adenovirus serotypes (Ad3, Ad7, Ad11, and Ad14) that use receptor(s) other than coxsackie-adenovirus receptor and CD46 were able to trigger EMT in epithelial ovarian cancer cells and cause efficient oncolysis. Our studies on ovarian cancer cultures and xenografts also revealed several interesting cancer cell biology features. Tumors in situ as well as tumor xenografts in mice mostly contained epithelial cells and cells that were in a hybrid stage where they expressed both epithelial and mesenchymal markers (epithelial/mesenchymal cells). These epithelial/mesenchymal cells are the only xenograft-derived cells that can be cultured and with passaging undergo EMT and differentiate into mesenchymal cells. Our study provides a venue for improved virotherapy of cancer as well as new insights into cancer cell biology.

| S-EPMC2738419 | biostudies-literature