Long non-coding RNA HOTAIR acts as a competing endogenous RNA to promote malignant melanoma progression by sponging miR-152-3p
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Wenkang Luan1,*, Rubo Li2,*, Liang Liu3,*, Xin Ni4,*, Yan Shi3, Yun Xia1, Jinlong Wang1, Feng Lu1 and Bin Xu1
1Department of Plastic Surgery, Affiliated People's Hospital of Jiangsu University, Zhenjiang, China
2Department of Neurosurgery, Affiliated People's Hospital of Jiangsu University, Zhenjiang, China
3Department of Neurosurgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China
4Department of Gastroenterology, Affiliated Hospital of Jiangsu University, Zhenjiang, China
*These authors have contributed equally to this work
Wenkang Luan, email: [email protected]
Bin Xu, email: [email protected]
Keywords: malignant melanoma, ceRNA, HOTAIR, miR-152-3p, c-MET
Received: April 15, 2017 Accepted: July 12, 2017 Published: August 03, 2017
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.
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