Wang Pan, Hu Liu, Fu Guili, Lu Jingjing, Zheng Yuanquan, Li Ying, Jia Lin
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.
Department of Radiotherapy, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, 430071, People's Republic of China.
Cancer Manag Res. 2020 Jul 29;12:6553-6562. doi: 10.2147/CMAR.S249348. eCollection 2020.
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.
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.
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.
lncRNA MALAT1 promotes malignant proliferation of melanoma cells through miR-23a.
本研究旨在探讨长链非编码RNA转移相关肺腺癌转录本1(lncRNA MALAT1)/miR-23a-23a与黑色素瘤之间的关系。
收集52例相应的非肿瘤正常组织以及109例(包括62例原发性黑色素瘤和47例转移性黑色素瘤)。采用实时荧光定量PCR对lncRNA MALAT1和miR-23a进行定量,并统计高/低miR-23和高/低lncRNA MALAT1人群的3年生存率。根据lncRNA MALAT1和miR-23a的序列信息预测结合位点。构建lncRNA MALAT1 siRNA和miR-23a模拟载体,分别转染至黑色素瘤细胞系中,观察其对细胞的影响。
与相应的非肿瘤正常组织相比,黑色素瘤组织中lncRNA MALAT1升高而miR-23a降低。与原发性黑色素瘤相比,转移性黑色素瘤中lncRNA MALAT1更高而miR-23a更低。lncRNA MALAT1的下调导致miR-23a上调,且lncRNA MALAT1可与miR-23a结合。下调lncRNA MALAT1或上调miR-23a均可抑制细胞增殖、迁移和侵袭,并促进细胞凋亡。挽救实验显示,miR-23a的下调可抵消lncRNA MALAT1下调引起的细胞变化。
lncRNA MALAT1通过miR-23a促进黑色素瘤细胞的恶性增殖。