Silencing of the type 1 insulin-like growth factor receptor increases the sensitivity to apoptosis and inhibits invasion in human lung adenocarcinoma A549 cells.
Silencing of the type 1 insulin-like growth factor receptor increases the sensitivity to apoptosis and inhibits invasion in human lung adenocarcinoma A549 cells.
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DOI：
10.2478/s11658-007-0022-1
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发表时间：
2007
影响因子：
8.3
通讯作者：
Qian J
中科院分区：
文献类型：
--
作者：
Ma Z;Dong A;Kong M;Qian J
1型胰岛素样生长因子受体（IGF-1 R）在许多人类癌症（包括肺癌）中过度表达或活化，介导癌细胞增殖和转移。一些研究表明，阻断IGF-1 R表达可以抑制肿瘤细胞增殖和转移。本研究发现，编码针对IGF-1 R的短发夹RNA的重组腺病毒抑制内源性IGF-1 R，可显着抑制A549细胞的IGF-1 R表达，阻滞细胞周期，增强细胞凋亡反应，并抑制A549细胞的增殖、粘附、侵袭和迁移。此外，沉默IGF-1 R降低了侵袭相关基因的表达，包括基质金属蛋白酶-2（MMP-2）、MMP-9和尿激酶-纤溶酶原激活物（u-PA），以及Akt和ERK 1/2的磷酸化。这些结果表明，IGF-1 R的沉默有可能成为一种有效的癌症基因治疗策略，对人类肺癌。
The type 1 insulin-like growth factor receptor (IGF-1R), which is over-expressed or activated in many human cancers, including lung cancer, mediates cancer cell proliferation and metastasis. Several studies indicate that blocking IGF-1R expression can inhibit tumor cell proliferation and metastasis. In this study, inhibition of the endogenous IGF-1R by recombinant adenoviruses encoding short hairpin RNAs against IGF-1R was found to significantly suppress IGF-1R expression, arrest the cell cycle, enhance the apoptotic response, and inhibit proliferation, adhesion, invasion and migration in A549 cells. Moreover, silencing IGF-1R decreases the expression of invasive-related genes including matrix metalloproteinase-2 (MMP-2), MMP-9, and urokinase-plasminogen activator (u-PA), and the phosphorylation of Akt and ERK1/2. These results suggest that the silencing of IGF-1R has the potential to be an effective cancer gene therapy strategy for human lung cancer.
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影响因子：
4.6
作者：
Mezzetti, M;Panigalli, T;Meda, S
通讯作者：
Meda, S
影响因子：
6.4
作者：
Chernicky, CL;Yi, LJ;Ilan, J
通讯作者：
Ilan, J
DOI：
10.1073/pnas.210394297
发表时间：
2000-10-24
影响因子：
11.1
作者：
Playford, MP;Bicknell, D;Macaulay, VM
通讯作者：
Macaulay, VM
影响因子：
5.3
作者：
KALEKO, M;RUTTER, WJ;MILLER, AD
通讯作者：
MILLER, AD
影响因子：
1.4
作者：
Ma, J;Pollak, M;Stampfer, MJ
通讯作者：
Stampfer, MJ