Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22.

// Wenkang Luan 1, * , Lubo Li 2, * , Yan Shi 4, * , Xuefeng Bu 3 , Yun Xia 1 , Jinlong Wang 1 , Henry Siaw Djangmah 1 , Xiaohui Liu 1 , Yongping You 5 , Bin Xu 1 1 Department of Plastic Surgery, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China 2 Department of Neurosurgery, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China 3 Department of General Surgery, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China 4 Department of Neurosurgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China 5 Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China * These authors have contributed equally to this work Correspondence to: Wenkang Luan, email: luanwenkang@126.com Bin Xu, email: xubinfen@126.com Keywords: MALAT1, miR-22, MMP14 and Snail, ceRNA, melanoma Received: June 03, 2016      Accepted: August 13, 2016      Published: August 24, 2016 ABSTRACT Long non-coding RNAs (lncRNAs) are involved in tumorigenesis. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), an lncRNAs, is associated with the growth and metastasis of many human tumors, but its biological roles in malignant melanoma remain unclear. In this study, the aberrant up-regulation of MALAT1 was detected in melanoma. We determined that MALAT1 promotes melanoma cells proliferation, invasion and migration by sponging miR-22. MiR-22 was decreased and acted as a tumor suppressor in melanoma, and MMP14 and Snail were the functional targets of miR-22. Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22. The effects of MALAT1 in malignant melanoma is verified using a xenograft model. This finding elucidates a new mechanism for MALAT1 in melanoma development and provides a potential target for melanoma therapeutic intervention.