Abstract
The existence of several model systems with which to investigate a particular disease is advantageous for researchers. This is especially true for ovarian cancer, which, due to its complex and heterogeneous nature, inherently requires a large number of model systems. Here, we report a new ovarian serous adenocarcinoma cell line, designated YDOV-157, and characterized via post genomics and post proteomics. In this study, primary culture of tumor cells from ascites was performed and the cells were immortalized up to at least 60 passages in vitro. We studied the morphologies, cell proliferation, BRCA1/2 mutations, tumorigenesis capacity, and chemosensitivity of YDOV-157. Using a cDNA microarray, differentially expressed genes were identified and some of them were validated. Using proteomic analysis, we identified proteins that were differentially expressed in YDOV-157. The newly derived cell line, designated YDOV-157, grew as a monolayer and the doubling time was 102 h. When transplanted into nude mice, it initiated the formation of tumor masses with microscopic findings identical to those of the primary tumor. Chemosensitivity test showed that paclitaxel induced the highest chemosensitivity index. In microarray analysis, 2,520 probes were differently expressed, compared to human ovarian surface epithelial cells (HOSEs). In SYBR Green real-time PCR, the expression of E2F2 (P = 0.040) and CRABP2 genes (P = 0.030) was significantly higher in the ovarian cancer cell lines than in HOSEs. Furthermore, proteomic analysis showed that expression of 28 spots was significantly altered between YDOV-157 and HOSE. In conclusion, the newly derived YDOV-157 cell line may be an important research resource for studying cancer cell biology and should also be very useful for developing new strategies that inhibit cancer cell growth and progression.
Original language | English |
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Pages (from-to) | 189-201 |
Number of pages | 13 |
Journal | Molecular and Cellular Biochemistry |
Volume | 319 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 2008 Dec |
Bibliographical note
Funding Information:Acknowledgments This work was supported in part by National R&D Program for Cancer Control, Ministry of Health and Welfare, Republic of Korea (7-2006-0153), CMB-YUHAN research grant of Yonsei University College of Medicine for 2006 (6-2006-0030), and the Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund) (KRF-2006-311-e00339).
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Clinical Biochemistry
- Cell Biology