Non-small cell lung cancer is susceptible to induction of DNA damage responses and inhibition of angiogenesis by telomere overhang oligonucleotides.
Non-small cell lung cancer is susceptible to induction of DNA damage responses and inhibition of angiogenesis by telomere overhang oligonucleotides.
复制标题
DOI：
10.1016/j.canlet.2013.09.010
复制
发表时间：
2014-02-01
期刊：
影响因子：
9.7
通讯作者：
Salgia R
中科院分区：
文献类型：
--
作者：
Puri N;Pitman RT;Mulnix RE;Erickson T;Iness AN;Vitali C;Zhao Y;Salgia R
端粒突出端的暴露作为DNA损伤信号，外源性给予与3′-端粒突出端序列同源的11个碱基的寡核苷酸（T-oligo）通过诱导非小细胞肺癌（NSCLC）细胞的衰老和细胞死亡来模拟突出端暴露的作用，但在正常支气管上皮细胞中则不然。T-oligo诱导的NSCLC细胞增殖减少可能通过p53及其同源物p73，以及随后在体内和体外诱导衰老和衰老相关蛋白p21，p33 ING和p27 Kip 1的表达来指导。此外，T-oligo通过降低VEGF信号传导和增加TSP-1表达来减小肿瘤大小并抑制血管生成。
Exposure of the telomere overhang acts as a DNA damage signal, and exogenous administration of an 11-base oligonucleotide homologous to the 3′-telomere overhang sequence (T-oligo) mimics the effects of overhang exposure by inducing senescence and cell death in non-small cell lung cancer (NSCLC) cells, but not in normal bronchial epithelial cells. T-oligo-induced decrease in cellular proliferation in NSCLC is likely directed through both p53 and its homolog, p73, with subsequent induction of senescence and expression of senescence-associated proteins, p21, p33ING, and p27Kip1 both in vivo and in vitro. Additionally, T-oligo decreases tumor size and inhibits angiogenesis through decreased VEGF signaling and increased TSP-1 expression.
登录
查看更多内容
宇宙（癌症中的体细胞突变目录）数据库和网站。
影响因子：
8.8
作者：
Bamford, S;Dawson, E;Forbes, S;Clements, J;Pettett, R;Dogan, A;Flanagan, A;Teague, J;Futreal, PA;Stratton, MR;Wooster, R
通讯作者：
Wooster, R
影响因子：
8.8
作者：
通讯作者：
--
影响因子：
3.4
作者：
Chatelut, E;Delord, JP;Canal, P
通讯作者：
Canal, P
DOI：
10.1073/pnas.92.20.9363
发表时间：
1995-09-26
影响因子：
11.1
作者：
DIMRI, GP;LEE, XH;CAMPISI, J
通讯作者：
CAMPISI, J
影响因子：
8
作者：
Jung, MS;Yun, J;Shin, DY
通讯作者：
Shin, DY