长链非编码 RNA MIAT 的表达下调通过 PI3K/AKT 信号通路抑制黑色素瘤的迁移和侵袭。
Downregulation of the expression of the lncRNA MIAT inhibits melanoma migration and invasion through the PI3K/AKT signaling pathway.
机构信息
Department of Ophthalmology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan 610072, China.
Department of Ophthalmology, Eye Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.
出版信息
Cancer Biomark. 2019;24(2):203-211. doi: 10.3233/CBM-181869.
BACKGROUND
Long noncoding RNA MIAT expression is related to the development of some diseases. However, the role of MIAT in melanoma was has seldom been studied.
OBJECTIVE
To investigate the effect of the lncRNA MIAT on melanoma cells.
METHOD
Microarray was used to analyze the lncRNAs expression in tissue samples. The expression of the lncRNA MIAT was detected by qRT-PCR. A CCK-8 assay was used to assess cell viability, and cell counting was used to analyze cell proliferation. Wound healing and Transwell invasion assays were used to detect the migration and invasion abilities, respectively, of melanoma cells. Western blotting was performed to explore the molecular mechanisms of MIAT in melanoma.
RESULTS
The lncRNA MIAT was overexpressed in melanoma. The overexpression of MIAT promoted cell proliferation, cell invasion and migration, while the knockdown of MIAT expression got the opposite results. MIAT significantly upregulated the phosphorylation of PI3K and AKT and promoted cMyc and cyclin D1 protein expression.
CONCLUSION
LncRNA MIAT was a key factor to promote cell invasion, migration and proliferation through the PI3K/AKT signaling pathway. These findings may give us a potential way to treat melanoma.
背景
长链非编码 RNA MIAT 的表达与一些疾病的发展有关。然而，MIAT 在黑色素瘤中的作用很少被研究。
目的
探讨 lncRNA MIAT 对黑色素瘤细胞的影响。
方法
使用微阵列分析组织样本中的 lncRNA 表达。通过 qRT-PCR 检测 lncRNA MIAT 的表达。使用 CCK-8 测定法评估细胞活力，并用细胞计数分析细胞增殖。通过划痕愈合和 Transwell 侵袭实验分别检测黑色素瘤细胞的迁移和侵袭能力。通过 Western blot 实验探索 MIAT 在黑色素瘤中的分子机制。
结果
lncRNA MIAT 在黑色素瘤中过表达。MIAT 的过表达促进了细胞增殖、细胞侵袭和迁移，而 MIAT 表达的下调则得到了相反的结果。MIAT 显著上调了 PI3K 和 AKT 的磷酸化水平，并促进了 cMyc 和 cyclin D1 蛋白的表达。
结论
lncRNA MIAT 是通过 PI3K/AKT 信号通路促进细胞侵袭、迁移和增殖的关键因素。这些发现可能为我们提供了一种治疗黑色素瘤的潜在方法。
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