Department of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Department of Pharmacy, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Thorac Cancer. 2020 Sep;11(9):2681-2689. doi: 10.1111/1759-7714.13605. Epub 2020 Aug 6.
Long non-coding RNA-urothelial carcinoma associated 1 (LncRNA-UCA1) is a crucial oncogene that is deregulated in many types of cancers. However, the mechanism of UCA1 function, especially for its posttranscriptional regulation in lung cancer, remains unclear.
miRCode was used to predict potential miRNA candidates that might target UCA1. The targets of miR-138 and miR-193 on UCA1 and CDK6 were verified by luciferase reporter analysis. Western blotting was used to detect protein levels. The RNA level was evaluated using quantitative real-time polymerase chain reaction (PCR). Proliferation, wound healing, and transwell invasion assays were performed to assess cell proliferation and invasion abilities. Correlations between miR-138 or miR-193 and UCA1 in lung cancer tissues was assessed using quantitative real-time PCR.
miR-138 and miR-193 specifically targeted and regulated lncRNA-UCA1. MiR-138 and miR-193 both suppressed cell proliferation and cell cycle progression. Moreover, miR-138 and miR-193 inhibited cell migration and invasion. Overexpression of UCA1 reversed the proliferation, migration, and invasion suppression effects of miR-138 or miR-193. Furthermore, miR-138/193 affected the expression of UCA1 downstream genes. UCA1 regulated the expression of CDK6 as a miR-138 and miR-193 common target. In human lung cancer tissues, our study showed a significant negative correlation between miR-138 or miR-193 and UCA1 in lung cancer tissues.
Our results demonstrated that miR-138 and miR-193 affect cell function by directly targeting and regulating UCA1 in lung cancer.
长链非编码 RNA-尿路上皮癌相关 1（LncRNA-UCA1）是一种重要的癌基因，在许多类型的癌症中都失调。然而，UCA1 功能的机制，特别是其在肺癌中的转录后调控机制仍不清楚。
使用 miRCode 预测可能靶向 UCA1 的潜在 miRNA 候选物。通过荧光素酶报告分析验证 miR-138 和 miR-193 对 UCA1 和 CDK6 的靶标。使用 Western blot 检测蛋白水平。使用定量实时聚合酶链反应（PCR）评估 RNA 水平。进行增殖、划痕愈合和 Transwell 侵袭实验以评估细胞增殖和侵袭能力。使用定量实时 PCR 评估肺癌组织中 miR-138 或 miR-193 与 UCA1 的相关性。
miR-138 和 miR-193 特异性靶向并调节 lncRNA-UCA1。miR-138 和 miR-193 均抑制细胞增殖和细胞周期进程。此外，miR-138 和 miR-193 抑制细胞迁移和侵袭。UCA1 的过表达逆转了 miR-138 或 miR-193 的增殖、迁移和侵袭抑制作用。此外，miR-138/193 影响 UCA1 下游基因的表达。UCA1 作为 miR-138 和 miR-193 的共同靶标调节 CDK6 的表达。在人类肺癌组织中，我们的研究表明 miR-138 或 miR-193 与肺癌组织中 UCA1 的表达呈显著负相关。
我们的结果表明，miR-138 和 miR-193 通过直接靶向和调节肺癌中的 UCA1 来影响细胞功能。
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