Downregulation of LRIG2 expression by RNA interference inhibits glioblastoma cell (GL15) growth, causes cell cycle redistribution, increases cell apoptosis and enhances cell adhesion and invasion in vitro
Downregulation of LRIG2 expression by RNA interference inhibits glioblastoma cell (GL15) growth, causes cell cycle redistribution, increases cell apoptosis and enhances cell adhesion and invasion in vitro
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通过RNA干扰下调LRIG2表达可抑制胶质母细胞瘤细胞（GL15）生长，引起细胞周期重新分配，增加细胞凋亡并增强细胞体外粘附和侵袭
DOI：
10.4161/cbt.8.11.8375
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发表时间：
2009-06-01
影响因子：
3.6
通讯作者：
Guo, Dongsheng
中科院分区：
文献类型：
--
作者：
Wang, Baofeng;Han, Lin;Guo, Dongsheng
富含亮氨酸和免疫球蛋白样结构域（LRIG）基因家族包含LRIG1、2和3。LRIG1是EGFR的负调控因子，但对LRIG2的功能知之甚少。为了确定LRIG2在胶质瘤进展中的作用，我们在人胶质瘤细胞系（GL15）中进行了RNA干扰介导的LRIG2敲低。LRIG2表达下调导致：egf介导的EGFR快速丢失；减少扩散;G (0) / G(1)被捕;自发凋亡增加；增强GL15细胞的粘附能力和体外侵袭能力。这些发现表明LRIG2与LRIG1相比具有不同的功能，并验证了LRIG2作为胶质瘤治疗靶点的吸引力。
The leucine-rich and immunoglobulin-like domains (LRIG) gene family contains LRIG1, 2 and 3. LRIG1 is a negative regulator of EGFR, but little is known about the function of LRIG2. To determine the role of LRIG2 in the progression of glioma, we performed RNA interference-mediated knockdown of LRIG2 in a human glioma cell line (GL15). Downregulation of LRIG2 expression resulted in: rapid EGF-mediated loss of EGFR; decreased proliferation; G(0)/G(1) arrest; increased spontaneous apoptosis; enhanced cell adhesion and increased invasion capability of GL15 cells in vitro. These findings indicate that LRIG2 possesses distinct functions compared with LRIG1 and validate the attractiveness of LRIG2 as a target in glioma therapy.