| lncRNA CERS6-AS1 通过调控 miR-138-2-3p 抑制人胶质瘤细胞系增殖 |
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| 引用本文： | 黄琦,翟海程.lncRNA CERS6-AS1 通过调控 miR-138-2-3p 抑制人胶质瘤细胞系增殖[J].医学分子生物学杂志,2023,20(1):20-25. |
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| 作者姓名： | 黄琦 翟海程 |
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| 作者单位： | 汉中市中心医院神经外科 陕西省汉中市, 723000 |
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| 基金项目： | 汉中市中心医院科研项目 (No. YK1807) |
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| 摘 要： | 目的 探讨 lncRNA CERS6-AS1 对胶质瘤细胞生物学行为的影响及其可能作用机制。 方法 qRT-PCR 法检测胶质瘤组织、 癌旁组织中 CERS6-AS1 和 miR-138-2-3p 的表达量; Pearson 法分析胶质瘤组织中
CERS6-AS1 与 miR-138-2-3p 表达量的相关性; 体外培养人胶质瘤细胞 T98G, 将 si-NC、 si-CERS6-AS1、 miR-NC、 miR-138-2-3p mimics、 si-CERS6-AS1 与 anti-miR-NC、 si-CERS6-AS1 与 anti-miR-138-2-3p 分 别 转 染 至
T98G 细胞; CCK-8 法、 平板克隆形成实验、 Transwell 小室实验分别检测细胞增殖、 克隆形成、 迁移及侵袭
能力; 双荧光素酶报告基因实验检测 CERS6-AS1 和 miR-138-2-3p 的靶向关系。 结果 与癌旁组织比较, 胶
质瘤组织中 CERS6-AS1 的表达量升高 (P< 0. 05), miR-138-2-3p 的表达量降低 (P< 0. 05); CERS6-AS1 与
miR-138-2-3p 呈负相关 (r = - 0. 8899, P< 0. 001); si-CERS6-AS1 组细胞活力、 克隆形成细胞数、 迁移及侵
袭细胞数均低于 si-NC 组 (P< 0. 05); CERS6-AS1 可靶向调节 miR-138-2-3p 的表达; miR-138-2-3p 组细胞活
力、 克隆形成细胞数、 迁移及侵袭细胞数均少于 miR-NC 组 (P< 0. 05); si-CERS6-AS1 + anti-miR-138-2-3p
组细胞活力、 克隆形成细胞数、 迁移及侵袭细胞数均比 si-CERS6-AS1 + anti-miR-NC 组增多 (P< 0. 05)。 结论 干扰 CERS6-AS1 表达可通过调控 miR-138-2-3p 而抑制胶质瘤细胞增殖、 克隆形成、 迁移及侵袭。
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| 关 键 词： | lncRNA CERS6-AS1 miR-138-2-3p 胶质瘤 细胞增殖 侵袭 |
lncRNA CERS6-AS1 Inhibits the Proliferation of Human Glioma Cell
Lines by Regulating miR-138-2-3p |
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| HUANG Qi,ZHAI Haicheng.lncRNA CERS6-AS1 Inhibits the Proliferation of Human Glioma Cell
Lines by Regulating miR-138-2-3p[J].Journal of Medical Molecular Biology,2023,20(1):20-25. |
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| Authors: | HUANG Qi ZHAI Haicheng |
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| Affiliation: | Department of Neurosurgery, Hanzhong Central Hospital, Hanzhong, Shaanxi, 723000, China |
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| Abstract: | Objective To explore the effect of lncRNA CERS6-AS1 on the biological behavior
of glioma cells and its possible mechanism. Methods qRT-PCR method was used to detect the expression levels of CERS6-AS1 and miR-138-2-3p in glioma tissues and adjacent tissues. Pearson
method was used to analyze the correlation between CERS6-AS1 and miR-138-2-3p expression in glioma tissues. Human glioma cells T98G were cultured in vitro, and then were transfected with si-NC,
si-CERS6-AS1, miR-NC, miR-138-2-3p mimics, si-CERS6-AS1 and anti-miR-NC, si-CERS6-AS1
and anti-miR-138-2-3p. The CCK-8 method, plate colony formation experiment, and transwell assay
were used to detect the cell capabilities of proliferation, clone formation, migration and invasion. The dual luciferase reporter gene experiment was used to verify the targeting relationship between CERS6-AS1 and miR-138-2-3p. Results Compared with the adjacent tissues, the expression
level ofCERS6-AS1 in glioma tissues was increased (P< 0. 05), while the expression level of miR-138-2-3p was decreased (P< 0. 05). CERS6-AS1 was negatively correlated with miR-138-2-3p (r =
- 0. 8899, P< 0. 001). CERS6-AS1 could target the expression of miR-138-2-3p. The cell viability,
the number of colony forming cells, the number of migration and invasion cells in the si-CERS6-AS1group were lower than those in the si-NC group (P< 0. 05). The cell viability, the number of colony formed cells, the number of migrated and invasive cells in the miR-138-2-3p group were less
than those in the miR-NC group (P< 0. 05). The cell viability, the number of clone formed cells,
the number of migrated and invasive cells in the si-CERS6-AS1 + anti-miR-138-2-3p group were all
higher than those in the si-CERS6-AS1 + anti-miR-NC group (P< 0. 05). Conclusion Interference
of the expression of CERS6-AS1 could inhibit the proliferation, clone formation, migration and invasion of glioma cells by regulating miR-138-2-3p. |
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| Keywords: | lncRNA CERS6-AS1 miR-138-2-3p glioma cell proliferation invasion |
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