跪求英译中!不要在线翻译的,谢谢!Antigene peptide nucleic acid specifically inhibits MYCN expression in human neuroblastoma cells leading to cell growth inhibition and apoptosisRoberto Tonelli,Stefania Purgato,Consuelo Camerin,Raffaele Fr

跪求英译中!不要在线翻译的,谢谢!Antigene peptide nucleic acid specifically inhibits MYCN expression in human neuroblastoma cells leading to cell growth inhibition and apoptosisRoberto Tonelli,Stefania Purgato,Consuelo Camerin,Raffaele Fr
跪求英译中!不要在线翻译的,谢谢!
Antigene peptide nucleic acid specifically inhibits MYCN expression in human neuroblastoma cells leading to cell growth inhibition and apoptosis
Roberto Tonelli,Stefania Purgato,Consuelo Camerin,Raffaele Fronza,Fabrizio Bologna,Simone Alboresi,Monica Franzoni,Roberto Corradini,Stefano Sforza,Andrea Faccini,Jason M. Shohet,Rosangela Marchelli,and Andrea Pession Department of Pediatrics, University of Bologna,Sant’Orsola-Malpighi Hospital, Bologna, Italy; Department of Organic and Industrial Chemistry, University of Parma, Parma,Italy; and 3Center for Cell and Gene Therapy, Texas Children’s Cancer Center, Baylor College of Medicine, Houston, Texas
Abstract
We developed an antigene peptide nucleic acid (PNA) for
selective inhibition of MYCN transcription in neuroblastoma
cells, targeted against a unique sequence in the
antisense DNA strand of exon 2 of MYCN and linked at
its NH2 terminus to a nuclear localization signal peptide.
Fluorescence microscopy showed specific nuclear delivery
of the PNA in six human neuroblastoma cell lines: GI-LIN
and IMR-32 (MYCN-amplified/overexpressed); SJ-NKP
and NB-100 (MYCN-unamplified/low-expressed);
and GI-CA-N and GI-ME-N (MYCN-unamplified/unexpressed).
Antiproliferative effects were observable at
24 hours (GI-LI-N, 60%; IMR-32, 70%) and peaked at
72 hours (GI-LI-N, 80%; IMR-32, 90%; SK-N-KP, 60%;
NB-100, 50%); no reduction was recorded for GI-CA-N
and GI-ME-N (controls). In MYCN-amplified/overexpressed
IMR-32 cells and MYCN-unamplified/lowexpressed
SJ-N-KP cells, inhibition was recorded of
MYCN mRNA (by real-time PCR) and N-Myc (Western
blotting); these inhibitory effects increased over 3 days
after single treatment in IMR-32. Antigene PNA induced
G1-phase accumulation (39–53%) in IMR-32 and apoptosis
(56% annexin V–positive cells at 24 hours in
IMR-32 and 22% annexin V–positive cells at 48 hours
in SJ-N-KP). Selective activity of the PNA was shown
by altering three point mutations, and by the observation
that an antigene PNA targeted against the noncoding
DNA strand did not exert any effect. These findings
could encourage research into development of an
antigene PNA–based tumor-specific agent for neuroblastoma
(and other neoplasms) with MYCN expression.
[Mol Cancer Ther 2005;4(5):779–86]

跪求英译中!不要在线翻译的,谢谢!Antigene peptide nucleic acid specifically inhibits MYCN expression in human neuroblastoma cells leading to cell growth inhibition and apoptosisRoberto Tonelli,Stefania Purgato,Consuelo Camerin,Raffaele Fr
抗原肽核酸抑制MYCN具体表达的神经母细胞瘤细胞,导致细胞生长的抑制和凋亡
　　罗伯托利,斯特凡Purgato ,苏埃洛卡默琳,拉菲尔Fronza ,梅奥尼博洛尼亚,西蒙娜Alboresi ,莫妮卡弗兰索尼,罗伯托Corradini ,斯特凡诺斯福尔扎,安德烈Faccini ,杰森先生Shohet ,Rosangela Marchelli ,和安德烈Pession儿科,博洛尼亚大学,圣' Orsola -马尔皮基医院,博洛尼亚,意大利;有机部和工业大学化学帕尔马,帕尔马,意大利和3Center的细胞和基因治疗,德州儿童癌症中心,Baylor医学院,得克萨斯州休斯敦
　　摘要
　　我们开发了一种抗原肽核酸（记者支林飞）的
　　选择性抑制神经母细胞瘤MYCN转录
　　细胞,针对一个独特的序列
　　反义DNA链的第2外显子,并与在MYCN
　　其氨基端为核定位信号肽.
　　荧光显微镜显示特定核运载
　　在巴民族权力机构在六个人类神经母细胞瘤细胞系：胃肠道林
　　和婴儿死亡率- 32 （ MYCN-amplified/overexpressed ） ;组SJ -新韩国党
　　和Nb - 100 （ MYCN-unamplified/low-expressed ） ;
　　和胃肠钙N和胃肠- ME公司氮（ MYCN-unamplified/unexpressed ） .
　　抗时可观察到效果
　　24小时（李基李氮,60 ％ ;婴儿死亡率- 32 ,70 ％ ） ,达到了
　　72小时（李基李氮,80 ％ ;婴儿死亡率- 32 ,90 ％ ; SK队氮金伯利进程,60 ％ ;
　　注：- 100 ,50 ％ ） ;没有减少录基晚上氮
　　和胃肠- ME公司氮（控制） .在MYCN-amplified/overexpressed
　　婴儿死亡率- 32细胞和MYCN-unamplified/lowexpressed
　　律政司司长氮金伯利进程细胞,抑制录的
　　MYCN基因（按实时PCR ）和N - myc基因（西
　　印迹） ;这些抑制效应增加了3天
　　单一的治疗后,婴儿死亡率32 .抗原诱导的巴勒斯坦民族权力机构
　　G1期阶段积累（ 39-53 ％ ）的婴儿死亡率- 32与细胞凋亡
　　（ 56 ％的膜联蛋白V阳性细胞在24小时内
　　婴儿死亡率,32和22 ％膜联蛋白V阳性细胞在48小时内
　　在组SJ - N一金伯利进程） .选择性活动表明巴勒斯坦民族权力机构
　　通过改变三个点突变,并通过观察
　　一个抗原机构针对非编码
　　DNA链没有施加任何影响.这些调查结果
　　可以鼓励研究发展的一个
　　抗原巴民族权力机构为基础的肿瘤特异性剂神经母细胞瘤
　　（和其他肿瘤）与MYCN表达.
　　[分子癌症有2005 ; 4 （ 5 ） :779 - 86 ]