Department of Clinical Laboratory, The Second Affiliated Hospital of Mudanjiang Medical University, Mudanjiang, Heilongjiang, P.R. China.
Department of Histology and Embryology, Mudanjiang Medical University, Mudanjiang, Heilongjiang, P.R. China.
Oncol Res. 2019 Feb 21;27(3):359-369. doi: 10.3727/096504018X15220594629967. Epub 2018 Apr 3.
This study aimed to explore the effects of lncRNA BCAR4 on the viability and aggressiveness of non-small cell lung cancer (NSCLC) cells. qRT-PCR was used to determine the expression of BCAR4 and downstream genes in NSCLC tissues and cell lines. Chromatin isolation by RNA purification (CHIRP) and Western blot were employed to measure the expression of the downstream proteins. Ki-67 expression in nude mice tumors was tested by immunohistochemistry. MTT assay, wound healing assay, and Transwell assay were used to assess NSCLC cell viability and aggressiveness, respectively. Tumor xenograft was conducted to determine the effects of BCAR4 and on NSCLC tumorigenesis in vivo. The expression of BCAR4 in NSCLC tissues and cells was significantly higher than the normal level. The overexpression of BCAR4 promoted NSCLC cell viability, migration, and invasion. The suppression of BCAR4 and showed the opposite effects. The overexpression of BCAR4 led to an increase in the expression of downstream proteins, while the suppression of BCAR4 and reduced their expression. In a tumor xenograft assay, the tumors in mice of the BCAR4 group showed the biggest volume, while those in mice of the si-GLI2 group showed the smallest volume. Ki-67 showed much higher levels in the BCAR4 overexpression group but much lower levels in the si-GLI2 group. In summary, the cooperative mechanism of lncRNA BCAR4 and might provide a new opportunity for treating NSCLC.
本研究旨在探讨长链非编码 RNA BCAR4 对非小细胞肺癌(NSCLC)细胞活力和侵袭性的影响。qRT-PCR 用于检测 NSCLC 组织和细胞系中 BCAR4 和下游基因的表达。通过 RNA 纯化的染色质免疫沉淀(CHIRP)和 Western blot 测定下游蛋白的表达。免疫组织化学检测裸鼠肿瘤中 Ki-67 的表达。MTT 测定、划痕愈合测定和 Transwell 测定分别用于评估 NSCLC 细胞活力和侵袭性。肿瘤异种移植用于确定 BCAR4 和在体内对 NSCLC 肿瘤发生的影响。BCAR4 在 NSCLC 组织和细胞中的表达明显高于正常水平。BCAR4 的过表达促进 NSCLC 细胞活力、迁移和侵袭。BCAR4 的抑制和的抑制表现出相反的效果。BCAR4 的过表达导致下游蛋白表达增加,而 BCAR4 的抑制和的抑制则降低其表达。在肿瘤异种移植试验中,BCAR4 组小鼠的肿瘤体积最大,而 si-GLI2 组小鼠的肿瘤体积最小。Ki-67 在 BCAR4 过表达组中的表达水平较高,而在 si-GLI2 组中的表达水平较低。总之,lncRNA BCAR4 和的协同机制可能为治疗 NSCLC 提供新的机会。