Conclusion
lncRNA MALAT1 promotes malignant proliferation of melanoma cells through miR-23a.
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.
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
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.