Department of Thoracic Surgery, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, China.
Eur Rev Med Pharmacol Sci. 2019 Oct;23(20):8878-8887. doi: 10.26355/eurrev_201910_19283.
The aim of this study was to investigate the expression level of long non-coding RNA (lncRNA) CASC11 in esophageal carcinoma (ECa), and to further explore its relationship with clinical progression, pathological parameters, and prognosis of ECa patients.
Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to examine the level of lncRNA CASC11 in 45 pairs of ECa tissues and adjacent normal tissues. The relationship between the lncRNA CASC11 level and clinical progression, pathological parameters, and prognosis of ECa patients was analyzed. Meanwhile, the level of lncRNA CASC11 in the ECa cell lines was verified by qPCR as well. In addition, lncRNA CASC11 knockdown model was constructed using lentiviral transfection in ECa cell lines. Subsequently, the cell counting kit-8 (CCK8), colony formation assay, and flow cytometry were used to explore the effect of lncRNA CASC11 on the biological functions of the ECa cells. Finally, the Western Blot and the recovery experiments were used to explore the potential mechanism.
In this work, the qPCR results showed that the expression level of lncRNA CASC11 in the ECa tissues was remarkably higher than that of the adjacent normal tissues, and the difference was statistically significant (p<0.05). Compared with patients with a low level of lncRNA CASC11, the pathological stage of patients with high expression was significantly higher, while the overall survival rate was lower (p<0.05). Compared with negative control (NC) group, the proliferation ability of the cells in the lncRNA CASC11 knockdown group CASC11 significantly decreased, whereas cell apoptosis remarkably increased (p<0.05). The Western Blot results revealed that protein expression of KLF6 was remarkably up-regulated after lncRNA CASC11 knockdown. In addition, the recovery experiments found that lncRNA CASC11 and KLF6 had mutual regulation, thereby promoting the malignant progression of ECa.
LncRNA CASC11 expression was remarkably up-regulated in ECa, which was associated with the pathological stage and poor prognosis of ECa. In addition, lncRNA CASC11 could promote the malignant progression of ECa by mutual regulation of KLF6.
本研究旨在探讨长链非编码 RNA（lncRNA） CASC11 在食管癌（ECa）中的表达水平，并进一步探讨其与 ECa 患者临床进展、病理参数和预后的关系。
采用实时定量聚合酶链反应（qRT-PCR）检测 45 对 ECa 组织和癌旁正常组织中 lncRNA CASC11 的水平。分析 lncRNA CASC11 水平与 ECa 患者临床进展、病理参数和预后的关系。同时，通过 qPCR 验证 ECa 细胞系中 lncRNA CASC11 的水平。此外，采用慢病毒转染构建 ECa 细胞系中的 lncRNA CASC11 敲低模型。随后，采用细胞计数试剂盒-8（CCK8）、集落形成实验和流式细胞术探讨 lncRNA CASC11 对 ECa 细胞生物学功能的影响。最后，采用 Western Blot 和恢复实验探讨潜在机制。
本研究中，qPCR 结果显示，lncRNA CASC11 在 ECa 组织中的表达水平明显高于癌旁正常组织，差异具有统计学意义（p<0.05）。与 lncRNA CASC11 低表达患者相比，高表达患者的病理分期明显较高，而总生存率较低（p<0.05）。与阴性对照（NC）组相比，lncRNA CASC11 敲低组细胞的增殖能力显著降低，而细胞凋亡显著增加（p<0.05）。Western Blot 结果显示，lncRNA CASC11 敲低后 KLF6 蛋白表达显著上调。此外，恢复实验发现，lncRNA CASC11 和 KLF6 相互调节，从而促进 ECa 的恶性进展。
lncRNA CASC11 在 ECa 中表达显著上调，与 ECa 的病理分期和预后不良有关。此外，lncRNA CASC11 可能通过相互调节 KLF6 促进 ECa 的恶性进展。
