Department of The First Thoracic Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Eur Rev Med Pharmacol Sci. 2018 Dec;22(23):8343-8352. doi: 10.26355/eurrev_201812_16532.
Accounting for 25% of all the cancers and 20% of the cancer-related mortality, lung cancer is one of the devastating types of cancers. Due to an increase in the incidence of lung cancer and limited treatment options, there is a pressing need to look for novel drug options and to identify potential therapeutic targets. Long non-coding RNAs (LncRNAs) have been considered to be important therapeutic targets due to their plethora of cellular roles. Herein, we investigated the therapeutic potential of UCA1 in lung cancer and also attempted to examine the underlying mechanism through UCA1 exerts its growth inhibitory effects on cancer cells.
The quantitative Reverse-Transcriptase Polymerase Chain Reaction (qRT-PCR) was used to perform the expression analysis. The CCK-8 assay was used to monitor the growth of the cells. The AO/EB assay was used to check apoptosis and flow cytometry was used for cell cycle distribution. The wound heal and transwell assays were used to monitor the cell migration and invasion.
It was found that the lncRNA UCA was significantly (p < 0.05) upregulated in the lung cancer cells and silencing of UCA1 could inhibit the proliferation of the SK-MES-1 lung cancer cells via induction of G2/M cell cycle arrest and apoptosis. Moreover, UCA1 silencing could also suppress the migration and invasion of the SK-MES-1 cells. The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells. Both UCA1 silencing and miR-143 overexpression could cause a significant decrease in the expression of mitogen-activated protein kinase 1 (MAPK1). Therefore, it is concluded that UCA1 regulates the growth of the SK-MES-1 lung cancer by inhibition of MAPK1 via miR-143 upregulation.
UCA1, as well as miR-143, may be essential therapeutic targets for the management of lung cancer and warrant further investigations.
肺癌占所有癌症的 25%和 20%的癌症相关死亡率，是一种具有破坏性的癌症类型。由于肺癌发病率的增加和治疗选择的有限，因此迫切需要寻找新的药物选择，并确定潜在的治疗靶点。长链非编码 RNA（lncRNA）因其众多的细胞功能而被认为是重要的治疗靶点。在此，我们研究了 UCA1 在肺癌中的治疗潜力，并试图通过研究 UCA1 对癌细胞生长抑制作用的潜在机制来检验其作用。
采用定量逆转录聚合酶链反应（qRT-PCR）进行表达分析。CCK-8 检测法用于监测细胞的生长情况。AO/EB 检测法用于检测细胞凋亡，流式细胞术用于检测细胞周期分布。划痕愈合和 Transwell 检测法用于监测细胞迁移和侵袭。
研究发现，lncRNA UCA 在肺癌细胞中显著上调（p < 0.05），沉默 UCA1 可通过诱导 G2/M 细胞周期阻滞和细胞凋亡来抑制 SK-MES-1 肺癌细胞的增殖。此外，沉默 UCA1 还可抑制 SK-MES-1 细胞的迁移和侵袭。还发现 LncRNA UCA1 可上调 miR-143 的表达，过表达 miR-143 也可抑制 SK-MES-1 肺癌细胞的增殖、迁移和侵袭。沉默 UCA1 和过表达 miR-143 均可显著降低丝裂原活化蛋白激酶 1（MAPK1）的表达。因此，UCA1 通过上调 miR-143 抑制 MAPK1 来调节 SK-MES-1 肺癌细胞的生长。
UCA1 和 miR-143 可能是肺癌管理的重要治疗靶点，值得进一步研究。
