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Objective:To explore the effect of inhibiting c-raf-1 by antisense technology on radiosensitivity in human cervical carcinoma cell line HeLa.Methods:There were four groups in the study:control group,lipofectin group,sense oligodexynucleotides(S-ODN) group,antisense oligodexynucleotides(AS-ODN) group.The expression of c-raf-1 was detected by means of RT-PCR,Cellular response to irradiation was evaluated by the colony forming test,Apoptosis was observed by fluorescent staining.Bcl-2 protein expression was determined by flow cytometry.Results:AS-ODN group could significantly decreased the proliferation rate and increasing the apoptosis rate,significantly downregulating the expression of Bcl-2 of irradiated human cervical carcinoma cells,(vs lipofectin group or S-ODN group,P
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Objective To investigate the mechanism of small-dose cisplatin in enhancing photodynamic therapy sensitivity and apoptosis in human cervical carcinoma cell lines.Methods The Hela and Siha cells were divided into four groups(blank control group,photodynamic therapy only,cisplatin only,photodynamic therapy and cisplatin).The effects on proliferation of Hela and Siha cells in the four groups were examined by MTT assay.The expression of P185c-erbB-2 in Hela and Siha cells affected was detected by immunocytochemistry.Results The degree of apoptosis caused by the joint application of cisplatin and photodynamic therapy was greater than that caused by cisplatin or photodynamic therapy alone.The expression of P185c-erbB-2 in cells declined correspondingly.However,the order of cisplatin and photodynamic therapy did not cause obvious differences in the effect.Conclusion The in vitro proliferation of Hela and Siha cells is restrained obviously by cisplatin combined with photodynamic therapy;the effect is greater than that of cisplatin or photodynamic therapy only.The mechanism of cispatin's enhancement of photodynamic therapy sensitivity may be related to inhibiting P185c-erbB-2 expression.
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Objective To investigate the correlation between methylation status and death-associated protein kinase 1 (DAPK1) in SiHa and Hela cell line of cervical carcinoma and intervention of DNA methyltransferase inhibitor 5-azacytidine on the expression of DAPK1 and the proliferation of the cells. Methods DAPK1 methylation status was analyzed using methylation-specific PCR methods. The expression of mRNA and protein of DAPK1 were analyzed by RT-PCR and SABC methods after the treatment with 5-azacytidine. MTT assay was used to observe the changes of proliferation activity of the cells after 5-azacytidine treatment. Results DAPK1 genes were methylated and did not express in SiHa cells in the cervical carcinoma. Its expression could be restored by 5-azacytidine. MTT assay showed 5-azacytidine could weaken the proliferation of cancerous cells. Conclusion DAPK1 methylation plays an important role in the carcinogenesis of cervical cells and can reexpress after the treatment with 5-azacytidine which also restored its inhibitory function on carcinoma.