长链非编码RNA MALAT1通过使miR-140沉默促进葡萄膜黑色素瘤细胞的生长和侵袭。
Long noncoding RNA MALAT1 promotes uveal melanoma cell growth and invasion by silencing of miR-140.
作者信息
Sun Lei, Sun Peng, Zhou Qi-Ying, Gao Xiangchun, Han Qing
机构信息
Department of Ophthalmology, The Fourth Hospital of Harbin Medical University Harbin 150001, Heilongjiang, China.
Department of Ophthalmology, The First Affiliated Hospital of Jiamusi University Jiamusi 154002, Heilongjiang, China.
出版信息
Am J Transl Res. 2016 Sep 15;8(9):3939-3946. eCollection 2016.
Increasing evidences have demonstrated that long noncoding RNAs (LncRNAs) play a significant role in the development of tumor. However, the role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in uveal melanoma remains unknown. In this study, we demonstrated that the expression of MALAT1 was upregulated in the uveal melanoma tissues compared to normal tissues. Among them, MALAT1 was upregulated in 72% (18/25) uveal melanoma tissues compared to their paired normal tissues. Knockdown of MALAT1 suppressed uveal melanoma cell proliferation, colony information, invasion and migration. Moreover, we showed that knockdown of MALAT1 promoted miR-140 expression and suppressed Slug and ADAM10 expression in the MUM-2C cell. In addition, we demonstrated that miR-140 was downregulated in the uveal melanoma tissues compared to normal tissues and cell lines. The expression level of MALAT1 was inversely correlated with the expression level of miR-140 in uveal melanoma tissues. These results suggested that MALAT1 served as an oncogenic LncRNA in the development of uveal melanoma.
越来越多的证据表明，长链非编码RNA（LncRNAs）在肿瘤发生发展中发挥着重要作用。然而，转移相关的肺腺癌转录本1（MALAT1）在葡萄膜黑色素瘤中的作用尚不清楚。在本研究中，我们发现与正常组织相比，MALAT1在葡萄膜黑色素瘤组织中的表达上调。其中，与配对的正常组织相比，72%（18/25）的葡萄膜黑色素瘤组织中MALAT1表达上调。敲低MALAT1可抑制葡萄膜黑色素瘤细胞的增殖、集落形成、侵袭和迁移。此外，我们发现敲低MALAT1可促进MUM-2C细胞中miR-140的表达，并抑制Slug和ADAM10的表达。另外，我们还发现与正常组织和细胞系相比，miR-140在葡萄膜黑色素瘤组织中表达下调。在葡萄膜黑色素瘤组织中，MALAT1的表达水平与miR-140的表达水平呈负相关。这些结果表明，MALAT1在葡萄膜黑色素瘤发生发展中作为一种致癌LncRNA发挥作用。
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