Abstract | PURPOSE: 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.
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Authors | Pan Wang, Liu Hu, Guili Fu, Jingjing Lu, Yuanquan Zheng, Ying Li, Lin Jia |
Journal | Cancer management and research
(Cancer Manag Res)
Vol. 12
Pg. 6553-6562
( 2020)
ISSN: 1179-1322 [Print] New Zealand |
PMID | 32801893
(Publication Type: Journal Article)
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Copyright | © 2020 Wang et al. |