Glioma is a lethal malignant brain tumor, which affects the brain functions and is life-threatening. LncRNA UCA1 was identified as a pivotal regulator for tumorigenesis of glioma. MiR-206 was discovered to promote tumorigenesis and is critical in the regulation of cell proliferation in glioma. This study will discuss the expression of UCA1 regarding miR-206 and CLOCK, and their integrative effects in the proliferation and cell cycle of glioma cells. qRT-PCR was conducted to measure the mRNA expressions of IgG and Ago2 in cells co-transfected with UCA1, and miR-216 in U251. Bioinformation was analyzed for the prediction of association between UCA1 and miR-206. Transwell migrations assays and invasion assays were utilized to observe the cell invasive ability. Western blot and immunofluorescence imaging were used to examine the protein expressions. In vivo comparisons and observations were also performed to investigate the role of UCA1 in glioma growth. LncRNA UCA1 was up-regulated in glioma cell lines and tissues. It elevated cell invasion via the inducing of epithelial-mesenchymal transition. We found that UCA1 can modulate miR-206 expression and serve as an endogenous sponge of miR-206. The EMT-inducer CLOCK was validated as a messenger RNA target of miR-206. At last, we demonstrated that UCA1 exerted the biology function through regulating miR-206 and CLOCK in vivo. Overall, the results demonstrated that UCA1/miR-206/CLOCK axis participated in the progressing of glioma and could act as a promising therapeutic target.

中文翻译：

---

LncRNA UCA1 通过 miR-206/CLOCK 轴促进胶质瘤中的细胞生长和侵袭

神经胶质瘤是一种致命的恶性脑肿瘤，它影响大脑功能并危及生命。LncRNA UCA1 被确定为胶质瘤肿瘤发生的关键调节因子。发现 MiR-206 可促进肿瘤发生，并且对调节胶质瘤细胞增殖至关重要。本研究将讨论UCA1在miR-206和CLOCK方面的表达，以及它们在胶质瘤细胞增殖和细胞周期中的综合作用。qRT-PCR 检测 UCA1 共转染细胞中 IgG 和 Ago2 的 mRNA 表达，以及 U251 中 miR-216 的 mRNA 表达。分析生物信息以预测 UCA1 和 miR-206 之间的关联。Transwell迁移试验和侵袭试验用于观察细胞侵袭能力。Western印迹和免疫荧光成像用于检查蛋白质表达。还进行了体内比较和观察，以研究 UCA1 在胶质瘤生长中的作用。LncRNA UCA1 在胶质瘤细胞系和组织中上调。它通过诱导上皮-间质转化提高细胞侵袭。我们发现 UCA1 可以调节 miR-206 的表达并作为 miR-206 的内源海绵。EMT 诱导子 CLOCK 被验证为 miR-206 的信使 RNA 靶标。最后，我们证明了UCA1通过在体内调节miR-206和CLOCK发挥生物学功能。总体而言，结果表明UCA1/miR-206/CLOCK轴参与了胶质瘤的进展，可以作为一个有前途的治疗靶点。它通过诱导上皮-间质转化提高细胞侵袭。我们发现 UCA1 可以调节 miR-206 的表达并作为 miR-206 的内源海绵。EMT 诱导子 CLOCK 被验证为 miR-206 的信使 RNA 靶标。最后，我们证明了UCA1通过在体内调节miR-206和CLOCK发挥生物学功能。总体而言，结果表明UCA1/miR-206/CLOCK轴参与了胶质瘤的进展，可以作为一个有前途的治疗靶点。它通过诱导上皮-间质转化提高细胞侵袭。我们发现 UCA1 可以调节 miR-206 的表达并作为 miR-206 的内源海绵。EMT 诱导子 CLOCK 被验证为 miR-206 的信使 RNA 靶标。最后，我们证明了UCA1通过在体内调节miR-206和CLOCK发挥生物学功能。总体而言，结果表明UCA1/miR-206/CLOCK轴参与了胶质瘤的进展，可以作为一个有前途的治疗靶点。我们证明了UCA1通过在体内调节miR-206和CLOCK发挥生物学功能。总体而言，结果表明UCA1/miR-206/CLOCK轴参与了胶质瘤的进展，可以作为一个有前途的治疗靶点。我们证明了UCA1通过在体内调节miR-206和CLOCK发挥生物学功能。总体而言，结果表明UCA1/miR-206/CLOCK轴参与了胶质瘤的进展，可以作为一个有前途的治疗靶点。