Pan Wang1, Liu Hu2, Guili Fu1, Jingjing Lu1, Yuanquan Zheng1, Ying Li2, Lin Jia3. 1. Department of Dermatology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science & Technology, Wuhan 430015, Hubei Province, People's Republic of China. 2. Department of Radiotherapy, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, 430071, People's Republic of China. 3. Department of Nephrology, The Central Hosptial of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430015, Hubei Province, People's Republic of China.
Abstract
PURPOSE: This study was designed to investigate the relationship between long-chain non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1)/miR-23a-23a and melanoma. PATIENTS AND METHODS: Fifty-two cases of corresponding non-tumor normal tissues and 109 cases (including 62 cases of primary melanoma and 47 cases of metastatic melanoma) were collected. Real-time fluorescent PCR quantified lncRNA MALAT1 and miR-23a, and counted the 3-year survival of high/low miR-23 and high/low lncRNA MALAT1 populations. We predicted the binding site according to the sequence information of lncRNA MALAT1 and miR-23a. lncRNA MALAT1 siRNA and miR-23a mimics vectors were constructed and transfected into melanoma cell lines respectively to observe their effects on cells. RESULTS: Compared with corresponding non-tumor normal tissues, lncRNA MALAT1 in melanoma tissue increased while miR-23a decreased. Compared with primary melanoma, metastatic melanoma was higher and miR-23a was lower. Downregulation of lncRNA MALAT1 caused upregulation of miR-23a, and lncRNA MALAT1 could bind to miR-23a. Downregulating lncRNA MALAT1 or upregulating miR-23a inhibited cell proliferation, migration and invasion and promoted apoptosis. Rescue experiments revealed that downregulation of miR-23a could offset cell changes caused by downregulation of lncRNA MALAT1. CONCLUSION: lncRNA MALAT1 promotes malignant proliferation of melanoma cells through miR-23a.
PURPOSE: This study was designed to investigate the relationship between long-chain non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1)/miR-23a-23a and melanoma. PATIENTS AND METHODS: Fifty-two cases of corresponding non-tumor normal tissues and 109 cases (including 62 cases of primary melanoma and 47 cases of metastatic melanoma) were collected. Real-time fluorescent PCR quantified lncRNA MALAT1 and miR-23a, and counted the 3-year survival of high/low miR-23 and high/low lncRNA MALAT1 populations. We predicted the binding site according to the sequence information of lncRNA MALAT1 and miR-23a. lncRNA MALAT1 siRNA and miR-23a mimics vectors were constructed and transfected into melanoma cell lines respectively to observe their effects on cells. RESULTS: Compared with corresponding non-tumor normal tissues, lncRNA MALAT1 in melanoma tissue increased while miR-23a decreased. Compared with primary melanoma, metastatic melanoma was higher and miR-23a was lower. Downregulation of lncRNA MALAT1 caused upregulation of miR-23a, and lncRNA MALAT1 could bind to miR-23a. Downregulating lncRNA MALAT1 or upregulating miR-23a inhibited cell proliferation, migration and invasion and promoted apoptosis. Rescue experiments revealed that downregulation of miR-23a could offset cell changes caused by downregulation of lncRNA MALAT1. CONCLUSION: lncRNA MALAT1 promotes malignant proliferation of melanoma cells through miR-23a.
Authors: Sean M Dawes; Sheena Tsai; Haley Gittleman; Jill S Barnholtz-Sloan; Jeremy S Bordeaux Journal: J Am Acad Dermatol Date: 2016-07-28 Impact factor: 11.527