Objective

Melanoma is a malignant skin cancer. This paper is dedicated to investigate the disease mechanism in regard to the axis of long noncoding RNA MAFG antisense 1 (MAFG-AS1)/microRNA (miR)-331-3p/KIT.

Methods

Levels of MAFG-AS1, miR-331-3p and KIT were analyzed in melanoma patients' cancer tissues and melanocytic nevi patients’ skin tissues. The correlation between prognosis of melanoma patients with MAFG-AS1 expression was observed. Loss- and gain-function tests were implemented to observe alternatives of cell biological activities.

Results

Melanoma patients’ cancer tissues expressed higher MAFG-AS1 and KIT and lower miR-331-3p. Patients with high MAFG-AS1 expression exhibited a poorer prognosis. After down-regulating MAFG-AS1 in A375 cells, cell proliferation, invasiveness, epithelial–mesenchymal transition (EMT) decreased, and apoptosis increased. Up-regulating MAFG-AS1 caused the opposite consequences. miR-331-3p inhibition or KIT overexpression eliminated the blockade of proliferation, invasion, and EMT caused by MAFG-AS1 silencing.

Conclusion

MAFG-AS1 competitively binds to miR-331-3p to elevate KIT expression, thereby enhancing the aggressiveness of melanoma cells.

中文翻译：

---

长非编码RNA MAFG-AS1通过竞争性结合miR-331-3p促进KIT表达，从而增强黑色素瘤细胞的增殖、侵袭和上皮-间质转化

客观的

黑色素瘤是一种恶性皮肤癌。本文致力于研究长非编码RNA MAFG反义1 (MAFG-AS1)/microRNA (miR)-331-3p/KIT轴的疾病机制。

方法

分析了黑色素瘤患者的癌症组织和黑色素细胞痣患者的皮肤组织中 MAFG-AS1、miR-331-3p 和 KIT 的水平。观察MAFG-AS1表达与黑色素瘤患者预后的相关性。进行丧失和获得功能测试以观察细胞生物活性的替代方案。

结果

黑色素瘤患者的癌症组织表达较高的 MAFG-AS1 和 KIT，表达较低的 miR-331-3p。MAFG-AS1 高表达的患者预后较差。在 A375 细胞中下调 MAFG-AS1 后，细胞增殖、侵袭、上皮间质转化 (EMT) 减少，细胞凋亡增加。上调 MAFG-AS1 会导致相反的结果。miR-331-3p 抑制或 KIT 过表达消除了 MAFG-AS1 沉默引起的增殖、侵袭和 EMT 阻断。

结论

MAFG-AS1 竞争性地结合 miR-331-3p 以提高 KIT 表达，从而增强黑色素瘤细胞的侵袭性。