Page 70 - 《中国药科大学学报》2026年第1期

64 学报 Journal of China Pharmaceutical University 2026, 57(1): 60 − 67 第 57 卷

A B A549 H1299
20 Vector 15 Vector
A549 H1299 ISM1 ISM1
Fold enrichment 10 Fold enrichment **
Plasmid Vector ISM1 Vector ISM1 15 ** 10
ISM1 60 kD 5 5

Tubulin 55 kD 0 0
0 24 48 72 0 24 48 72
t/h t/h
C D A549 H1299
A549 H1299 25 Vector 20 Vector
Cell lines Vector ISM1_OE Vector ISM1_OE 20 ISM1_OE ** 15 ISM1_OE **

ISM1 60 kD Fold enrichment 15 Fold enrichment 10
10
GAPDH 36 kD 5 5
0 0
0 24 48 72 96 0 24 48 72 96
t/h t/h
Figure 2 Overexpression of ISM1 suppressed the growth of NSCLCs ( x ± s, n=4)
A-B: A549 and H1299 cells were transfected with ISM1 plasmids or vector for 48 h. Then, cells were collected and subjected to Western blot, or
recultured and subjected to CCK-8 assay; C-D: ISM1 stable overexpression cell lines of A549 and H1299 (A549-ISM1_OE, H1299-ISM1_OE)
were established by infection with lentivirus carrying coding sequences of ISM1, and subsequent puromycin screening. Cells were subjected to
Western blot or CCK-8 assay
**P<0.01

Figure 3 rISM1 suppressed the growth of NSCLCs ( x ± s, n=4)
A549 cells (A) and H1299 cells (B) were treated with different concentrations of rISM1 for 24 h as indicated. Cells were subjected to CCK-8 assay
***P<0.001

3.5 rISM1 上调 FoxO3 和 FoxO1 表达，增加 ROS 是 p53 下游关键信号分子），而且 A549 细胞株具
产生，以及促进细胞凋亡 有 PTEN 基因突变，所以这两条信号通路可能在
针对上述转录组测序 KEGG 富集分析的结 rISM1 分子作用机制中不具有普遍意义。既往研究
果，即 rISM1 主要调控细胞周期、转录因子、p53 报道 FoxO1 和 FoxO3 在调控细胞周期、基因转录
和 FoxO 信号通路，对变化明显的基因进行了单独 表达以及脂代谢中都发挥重要作用，因此本研究
分析，结果显示抑癌信号分子基因 FoxO3、FoxO1、 首先关注了 FoxO1 和 FoxO3 的变化。qRT-PCR

CDKN1B （p27）、PTEN 的表达明显增加，而促癌信 结果显示，rISM1 处理显著上调 FoxO3 和 FoxO1 的
号分子基因 PIK3CD 的表达明显减少（图 5-A）。因 mRNA 表达（图 5-B）。Western blot 结果显示，rISM1
为 H1299 细胞是 p53 缺失突变的细胞株（CDKN1B 处理显著上调二者的蛋白表达（图 5-C）。既往研究