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作 者:阎炳智[1] 王洁[1] 张波[2] 董福生[3] 侯琳[2] 王旭[1]
机构地区:[1]河北医科大学口腔医学院口腔病理研究室,石家庄050017 [2]北京大学医学部病理系 [3]河北医科大学口腔医学院口腔颌面外科,石家庄050017
出 处:《中华口腔医学杂志》2006年第1期45-48,共4页Chinese Journal of Stomatology
基 金:国家自然科学基金资助项目(30271422);人事部留学回国人员科技活动择优基金资助项目;河北省自然科学基金资助项目(C2004000624)
摘 要:目的研究外源性野生型p53基因对涎腺腺样囊性癌细胞的抑制作用。方法构建携带野生型p53基因的腺病毒表达载体,以脂质体法转染涎腺腺样囊性癌SACC-83细胞,RT-PCR检测p53基因表达;采用TRAP-PCR-ELISA法检测转染细胞端粒酶活性,荧光素酶分析法检测人端粒酶逆转录酶基因(hTERT)启动子的转录;流式细胞术、软琼脂集落实验及裸鼠成瘤实验观察细胞生物特性的变化。结果外源性野生型p53基因导入使p53基因在涎腺腺样囊性癌细胞SACC-83中表达增强,其端粒酶活性降低、hTERT启动子转录抑制;转染细胞出现G1期阻滞,软琼脂集落形成率减少,裸鼠成瘤能力降低。结论腺病毒载体介导的外源性野生型p53基因可以抑制涎腺腺样囊性癌细胞端粒酶活性及细胞恶性表型。Objective To evaluate the inhibitory effect of p53 gene on salivary adenoid cystic carcinoma (SACC) cells. Methods Adenoviral vector pAEl-p53 was constructed and transfected into SACC-83 cells. The enhanced p53 expression was measured by reverse transcription polymerase chain reaction (RT-PCR), and the effects of transfected p53 on SACC-83 cells were analyzed by TRAP-PCRELISA, luciferase reporter, flow cytometry ( FCM), soft agar assay and tumorigenicity test. Results The expression of p53 gene in SACC-83 cells was increased after introduction of pAEl-p53. The telomerase activity and the transcriptional activity of hTERT promoter were inhibited. The cells cycles of transfected SACC-83 were arrested in G1 phase and the rate of colony-formation was decreased, and similarly the tumorigenicity in nude mice was also decreased. Conclusions The introduction of wild-type p53 by adenoviral vector could suppress the telomerase activity and malignant phenotypes of salivary adenoid cystic carcinoma cells.
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