Department of Radiation Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, China.
Eur Rev Med Pharmacol Sci. 2018 Dec;22(23):8333-8342. doi: 10.26355/eurrev_201812_16531.
The underlying mechanism of long non-coding RNA (lncRNA) in lung adenocarcinoma (LAC) has not been fully understood yet. Hence, this study aimed to determine the biological function of LINC00324 in LAC and to provide a novel diagnostic and therapeutic target for it.
The expression level of LINC00324 in 87 paired LAC tumor tissues and matched para-tumor tissues was detected using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay was employed to analyze the cell proliferative ability, whereas flow cytometry was performed to detect cell apoptotic rate. Cell metastasis change was measured using wound-healing assay and transwell assay. Luciferase reporter gene assay and Western blotting analysis were utilized to investigate the underlying mechanism of LINC00324 in LAC.
LINC00324 was highly expressed in LAC tissues compared with the para-tumor samples. Identically, the expression level of LINC00324 was significantly higher in LAC cell lines. The overexpression of LINC00324 promoted cell proliferation and inhibited cell apoptosis of LAC cells, while knockdown of LINC00324 presented the opposite effect. Up-regulation of LINC00324 accelerated cell migration and invasion, but down-regulation of LINC0324 decreased cell metastasis of LAC cells. Furthermore, miR-615-5p was found to be regulated by LINC00324 and inhibited AKT1 expression, indicating that LINC00324 promoted cell progression via affecting the miR-615-5p/AKT1 pathway.
LINC00324 was significantly over-expressed in LAC tissues and cells. It promoted proliferation and metastasis but inhibited cell apoptosis of LAC cells via sponging miR-615-5p to promote AKT1 expression. Our results demonstrated LINC00324 as a novel diagnostic and therapeutic target for LAC.
长链非编码 RNA（lncRNA）在肺腺癌（LAC）中的作用机制尚未完全阐明。因此，本研究旨在确定 LINC00324 在 LAC 中的生物学功能，并为其提供新的诊断和治疗靶点。
采用实时定量聚合酶链反应（qRT-PCR）检测 87 对 LAC 肿瘤组织和配对癌旁组织中 LINC00324 的表达水平。细胞计数试剂盒-8（CCK-8）检测分析细胞增殖能力，流式细胞术检测细胞凋亡率。划痕愈合实验和 Transwell 实验检测细胞转移变化。荧光素酶报告基因实验和 Western blot 分析用于研究 LINC00324 在 LAC 中的潜在作用机制。
与癌旁样本相比，LINC00324 在 LAC 组织中高表达。同样，LINC00324 在 LAC 细胞系中的表达水平也显著升高。LINC00324 的过表达促进了 LAC 细胞的增殖并抑制了细胞凋亡，而 LINC00324 的敲低则呈现相反的效果。上调 LINC00324 加速了 LAC 细胞的迁移和侵袭，但下调 LINC0324 则降低了 LAC 细胞的转移。此外，发现 LINC00324 调控 miR-615-5p 并抑制 AKT1 表达，表明 LINC00324 通过影响 miR-615-5p/AKT1 通路促进细胞进展。
LINC00324 在 LAC 组织和细胞中显著过表达。它通过海绵吸附 miR-615-5p 促进 AKT1 表达，促进 LAC 细胞的增殖和转移，抑制细胞凋亡。我们的研究结果表明，LINC00324 是 LAC 的一个新的诊断和治疗靶点。
