Liu Changhai, Ding Xiangsheng, Wei Cuie, Pei Yongdong, Meng Fanjun, Zhong Yuren, Liu Yi
Department of Burn and Plastic Surgery, The First Affiliated of Hospital of Kangda College of Nanjing Medical University/The First People's Hospital of Lianyungang, Lianyungang, People's Republic of China.
Department of Burn Plastic Surgery and Wound Repair, Second Hospital of Lanzhou University, Lanzhou, People's Republic of China.
Clin Cosmet Investig Dermatol. 2022 Apr 26;15:751-762. doi: 10.2147/CCID.S359786. eCollection 2022.
A cascade of genes and pathways have been reported in the precise regulation of malignant melanoma (MM). Previous study has demonstrated that lncRNA LNCOC1 is an oncogenic factor in the pathogenesis and development of various cancers. The present study explored the functionalities of LNCOC1 and its interactions with miR-124 in MM.
A total of 65 melanoma patients were enrolled in this study. The expression of LNCOC1 and miR-124 after cell transfection were detected by RT-qPCR. The migration rates of SK-MEL-3 and A375 cells after transient transfection with LNCOC1 expression vector and miR-124 mimic was detected by trans-well assay.
LNCOC1 was accumulated to high levels in melanoma, and it was significantly correlated with the low survival rate of melanoma patients. Our bioinformatics data showed that miR-124 could target LNCOC1. Overexpression of miR-124 could downregulate LNCOC1. However, up-regulated the expression of LNCOC1 did not affect the expression of miR-124. Our correlation analysis also revealed that the expression of LNCOC1 and miR-124 were inversely correlated in both melanoma tissues and non-tumor tissues. The trans-well invasion and migration assays indicated that overexpression of miR-124 inhibited the melanoma cell invasion and migration. However, overexpression of LNCOC1 promoted melanoma cell invasion and migration.
LNCOC1 is upregulated in melanoma, which can be considered as a potential target of miR-124 in modulating melanoma cell invasion and migration. LNCOC1 may also be an interfering target of MM therapy.
在恶性黑色素瘤（MM）的精确调控中，一系列基因和信号通路已被报道。先前的研究表明，lncRNA LNCOC1是多种癌症发病机制和发展中的致癌因子。本研究探讨了LNCOC1在MM中的功能及其与miR-124的相互作用。
本研究共纳入65例黑色素瘤患者。通过RT-qPCR检测细胞转染后LNCOC1和miR-124的表达。通过Transwell实验检测用LNCOC1表达载体和miR-124模拟物瞬时转染后SK-MEL-3和A375细胞的迁移率。
LNCOC1在黑色素瘤中积累至高水平，且与黑色素瘤患者的低生存率显著相关。我们的生物信息学数据表明，miR-124可以靶向LNCOC1。miR-124的过表达可下调LNCOC1。然而，上调LNCOC1的表达并不影响miR-124的表达。我们的相关性分析还显示，LNCOC1和miR-124的表达在黑色素瘤组织和非肿瘤组织中均呈负相关。Transwell侵袭和迁移实验表明，miR-124的过表达抑制黑色素瘤细胞的侵袭和迁移。然而，LNCOC1的过表达促进黑色素瘤细胞的侵袭和迁移。
LNCOC1在黑色素瘤中上调，可被视为miR-124调节黑色素瘤细胞侵袭和迁移的潜在靶点。LNCOC1也可能是MM治疗的干扰靶点。
