[Effects of DCC gene on cell growth and chemosensitivity of ovarian epithelial carcinoma cells].
OBJECTIVE
To study the effects of DCC gene transfection on cell-growth and chemosensitivity of ovarian epithelial carcinoma cell line HO8910.


METHODS
Recombinant eukaryotic expression vector pcDNA3.1(+)-DCC containing DCC gene was introduced by lipofectamine transfection reagent into ovarian epithelial carcinoma cell line HO8910 which does not express DCC endogenously. The expression of DCC was detected by RT-PCR and immunocytochemistry. The cell proliferation and the viability rate after different concentrations of cisplatin and paclitaxel were given were assessed by methyl thiazolyl tetrazolium (MTT) assay.


RESULTS
Exogenous DCC gene had been successfully transferred into HO8910 cells and obtained permanent expression. The growth speed of HO8910-DCC cells was significantly slower than other two groups. There was a significant difference between them (P < 0.01) except at the first day after being planted. There was no difference between the growth speed of HO8910 cells and that of HO8910-Neo cells (P > 0.05). The viability rate of HO8910-DCC cells was significantly lower than other two groups after (0.1 - 5.0) peak plasma concentration (PPC) of cisplatin and paclitaxel were given (P < 0.01). The viability rate of HO8910-DCC cells was lower than other two groups after 10.0 PPC concentration of cisplatin was given (P < 0.05), but there was no difference between them after 10.0 PPC concentration of paclitaxel was given (P > 0.05). The viability rate of HO8910 cells was similar to HO8910-Neo cells after different concentrations of cisplatin and paclitaxel were given (P > 0.05).


CONCLUSIONS
The DCC gene expression not only inhibits cell growth but also enhances the chemosensitity of ovarian epithelial carcinoma cell line HO8910.
Zhuang
Ru-Jin
RJ
Department of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Li
Pei-Ling
PL
Yu
Hai-Wei
HW
Li
Hui-Ming
HM
D000970:Antineoplastic Agents / Q000494:pharmacology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D002945:Cisplatin / Q000494:pharmacology*; D000075389:DCC Receptor; D004305:Dose-Response Relationship, Drug; D004354:Drug Screening Assays, Antitumor; D005260:Female; D005822:Genetic Vectors; D006801:Humans; D007150:Immunohistochemistry; D010051:Ovarian Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D017239:Paclitaxel / Q000494:pharmacology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000235:genetics* / Q000502:physiology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014162:Transfection / Q000379:methods; D025521:Tumor Suppressor Proteins / Q000096:biosynthesis / Q000235:genetics* / Q000502:physiology
D000970:Antineoplastic Agents; D000075389:DCC Receptor; C501909:DCC protein, human; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D025521:Tumor Suppressor Proteins; D017239:Paclitaxel; D002945:Cisplatin