Department of Medical Laboratory, Nanchong Central Hospital, Nanchong 637000, China.
J Healthc Eng. 2022 Mar 2;2022:9570900. doi: 10.1155/2022/9570900. eCollection 2022.
This paper aims to explore the lncRNA PROX1-AS1 effect on proliferation, migration, invasion, and apoptosis of lung cancer cells together with its targeted regulation on miR-1305. To adopt qRT-PCR to test PROX1-AS1 and miR-1305 expression levels in lung cancer tissues and adjacent tissues. Lung cancer cells A549 were cultured in vitro and randomly divided into several groups, which are si-NC, si-PROX1-AS1, miR-NC, miR-1305, si-PROX1-AS1 plus anti-miR-NC, and si-PROX1-AS1 plus anti-miR-1305. To adopt the CCK-8 method to test cell proliferation and to adopt the Transwell chamber experiment to test cell migration and invasion. To adopt the flow cytometry method to test the apoptosis rate. Through a dual luciferase experiment, we decided to find out the targeting relationship between PROX1-AS1 and miR-1305. Then we adopted the western blot method to test CyclinD1, MMP-2, MMP-9, Bcl-2, p21, and Bax expression levels. Compared with adjacent tissues ( < 0.05), the expression of PROX1-AS1 in lung cancer tissue was remarkably higher, while the expression of miR-1305 was remarkably lower ( < 0.05). After PROX1-AS1 knockdown expression or miR-1305 overexpression, cell activity, migration, and invasion ability were outstandingly lowered ( < 0.05), but the apoptosis rate was obviously raised ( < 0.05), CyclinD1, MMP-2, Bcl-2, and MMP-9 protein data were remarkably reduced ( < 0.05), but p21 and Bax protein conditions were outstandingly enhanced ( < 0.05). The dual luciferase experiment confirmed that PROX1-AS1 had a targeting relationship with miR-1305. After cotransfection with si-PROX1-AS1 and anti-miR-1305, the cell viability, migration and invasion ability were remarkably enhanced ( < 0.05), the apoptosis rate was remarkably reduced ( < 0.05), CyclinD1, MMP-2, Bcl-2, and MMP-9 protein were increased remarkably ( < 0.05), and p21 or Bax protein was lowered remarkably ( < 0.05). On the one hand, PROX1-AS1 can promote lung cancer proliferation, migration, and invasion. On the other hand, it may restrain apoptosis, possibly through inhibiting miR-1305 expression.
这篇论文旨在探讨 lncRNA PROX1-AS1 对肺癌细胞增殖、迁移、侵袭和凋亡的影响，以及其对 miR-1305 的靶向调节作用。采用 qRT-PCR 检测肺癌组织及癌旁组织中 PROX1-AS1 和 miR-1305 的表达水平。体外培养肺癌细胞 A549，随机分为 si-NC、si-PROX1-AS1、miR-NC、miR-1305、si-PROX1-AS1+anti-miR-NC 和 si-PROX1-AS1+anti-miR-1305 组。采用 CCK-8 法检测细胞增殖，采用 Transwell 室实验检测细胞迁移和侵袭，采用流式细胞术检测细胞凋亡率。通过双荧光素酶实验确定 PROX1-AS1 与 miR-1305 的靶向关系。采用 Western blot 法检测 CyclinD1、MMP-2、MMP-9、Bcl-2、p21 和 Bax 表达水平。与癌旁组织比较（ < 0.05），肺癌组织中 PROX1-AS1 表达明显升高，miR-1305 表达明显降低（ < 0.05）。PROX1-AS1 表达下调或 miR-1305 过表达后，细胞活性、迁移和侵袭能力明显降低（ < 0.05），但凋亡率明显升高（ < 0.05），CyclinD1、MMP-2、Bcl-2、MMP-9 蛋白数据明显减少（ < 0.05），但 p21 和 Bax 蛋白情况明显增强（ < 0.05）。双荧光素酶实验证实 PROX1-AS1 与 miR-1305 具有靶向关系。转染 si-PROX1-AS1 和 anti-miR-1305 后，细胞活力、迁移和侵袭能力明显增强（ < 0.05），凋亡率明显降低（ < 0.05），CyclinD1、MMP-2、Bcl-2、MMP-9 蛋白明显增加（ < 0.05），p21 或 Bax 蛋白明显减少（ < 0.05）。一方面，PROX1-AS1 可促进肺癌增殖、迁移和侵袭，另一方面可能通过抑制 miR-1305 表达来抑制细胞凋亡。
