ABSTRACT
<p><b>OBJECTIVE</b>To observe the protective effects of follicle stimulating hormone (FSH) on human epithelial ovarian cancer cell apoptosis induced by cisplatin (DDP).</p><p><b>METHODS</b>OVCAR3-FSHR cell were treated with DDP and FSH at serials of concentrations, MTT assay was used to examine the growth inhibition of OVCAR3-FSHR cell after treatment with DDP and FSH. Flow cytometry was used to analyze the change of cell cycle and percentage of apoptosis.</p><p><b>RESULTS</b>It was revealed that FSH decreased the growth inhibition induced by DDP. We also demonstrated that FSH reduced the S-phase percentage compared with the DDP only groups after treatment for 24 hours and reduced apoptosis percentage after 48 hours treatment with DDP.</p><p><b>CONCLUSION</b>It is suggested that FSH can protect the apoptosis induced by DDP. It also suggests that FSH may be an important chemoresistent reason for the chemotherapy of ovarian cancer.</p>
Subject(s)
Female , Humans , Antineoplastic Agents , Pharmacology , Apoptosis , Cisplatin , Pharmacology , Flow Cytometry , Follicle Stimulating Hormone , Pharmacology , Ovarian Neoplasms , Chemistry , Pathology , Receptors, FSH , Tumor Cells, CulturedABSTRACT
<p><b>OBJECTIVE</b>To investigate whether the follicle stimulating hormone (FSH) can inhibit apoptosis in ovarian cancer cells induced by cisplatin (DDP) and its possible mechinism.</p><p><b>METHODS</b>DNA fragmentation assay, (TdT-mediated dUTP nick end labling TUNEL), Western blot were used to analyze the changes in expression levels of Survivin and bcl-2 protein. The relative activity of caspase-3 was also determined.</p><p><b>RESULTS</b>200 mIU/ml FSH could regulate down the percentage of apoptotic cells and DNA fragmentation induced by 5.0 micrograms/ml cisplatin, while 200 mIU/ml FSH increased Survivin protein expression but could't influence the expression of bcl-2 protein.</p><p><b>CONCLUSION</b>FSH can inhibit ovarian cancer cells apoptosis induced by cisplatin. The possible mechinism is up-regulation of Survivin expression and down-regulation of caspase activity.</p>
Subject(s)
Female , Humans , Antineoplastic Agents , Pharmacology , Apoptosis , Caspase 3 , Caspases , Metabolism , Cisplatin , Pharmacology , DNA Fragmentation , Flow Cytometry , Follicle Stimulating Hormone , Pharmacology , Inhibitor of Apoptosis Proteins , Microtubule-Associated Proteins , Metabolism , Neoplasm Proteins , Ovarian Neoplasms , Metabolism , Pathology , Proto-Oncogene Proteins c-bcl-2 , Metabolism , Receptors, FSH , Metabolism , Tumor Cells, CulturedABSTRACT
<p><b>OBJECTIVE</b>To detect the trans-factors specifically binding to the strong enhancer element (GPEI) in the upstream of rat glutathione S-transferase P (GST-P) gene.</p><p><b>METHODS</b>Yeast one-hybrid system was used to screen rat lung MATCHMAKER cDNA library to identify potential trans-factors that can interact with core sequence of GPEI(cGPEI). Electrophoresis mobility shift assay (EMSA) was used to analyze the binding of transfactors to cGPEI.</p><p><b>RESULTS</b>cDNA fragments coding for the C-terminal part of the transcription factor c-Jun and rat adenine nucleotide translocator (ANT) were isolated. The binding of c-Jun and ANT to GPEI core sequence were confirmed.</p><p><b>CONCLUSIONS</b>Rat c-jun transcriptional factor and ANT may interact with cGPEI. They could play an important role in the induced expression of GST-P gene.</p>