Long non-coding RNA HOTAIR acts as a competing endogenous RNA to promote malignant melanoma progression by sponging miR-152-3p

被引:58
|
作者
Luan, Wenkang [1 ]
Li, Rubo [2 ]
Liu, Liang [3 ]
Ni, Xin [4 ]
Shi, Yan [3 ]
Xia, Yun [1 ]
Wang, Jinlong [1 ]
Lu, Feng [1 ]
Xu, Bin [1 ]
机构
[1] Jiangsu Univ, Affiliated Peoples Hosp, Dept Plast Surg, Zhenjiang, Peoples R China
[2] Jiangsu Univ, Affiliated Peoples Hosp, Dept Neurosurg, Zhenjiang, Peoples R China
[3] Nanjing Med Univ, Nanjing Hosp 1, Dept Neurosurg, Nanjing, Jiangsu, Peoples R China
[4] Jiangsu Univ, Affiliated Hosp, Dept Gastroenterol, Zhenjiang, Peoples R China
基金
中国国家自然科学基金;
关键词
malignant melanoma; ceRNA; HOTAIR; miR-152-3p; c-MET; CELL-GROWTH; CANCER; EXPRESSION; MECHANISMS; INSIGHTS; REVEALS; DOMAINS; MIRNAS; STATE;
D O I
10.18632/oncotarget.19910
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
HOX transcript antisense RNA (HOTAIR) is associated with the growth and metastasis of many human tumors, but its biological roles in malignant melanoma remain unclear. In this study, we show that HOTAIR is overexpressed in melanoma tissues and cells, especially in metastatic melanoma. High HOTAIR levels correlate with poor prognosis in melanoma patients. We also determined that HOTAIR functions as a competing endogenous RNA (ceRNA) for miR-152-3p. miR-152-3p was decreased and acted as a tumor suppressor in melanoma, and c-MET was the functional target of miR-152-3p. Furthermore, HOTAIR promotes the growth and metastasis of melanoma cells by competitively binding miR-152-3p, which functionally liberates c-MET mRNA and results in the activation of the downstream PI3k/Akt/mTOR signaling pathway. We determined that HOTAIR acts as a ceRNA to promote malignant melanoma progression by sponging miR-152-3p. This finding elucidates a new mechanism for HOTAIR in melanoma development and provides a potential therapeutic target for melanoma patients.
引用
收藏
页码:85401 / 85414
页数:14
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