Zhou Hong, Li Lingqiao, Wang Yingqian, Wang Dewei
Department of Plastic Surgery and Burn, The First People's Hospital of Changzhou, Changzhou, Jiangsu 213000, P.R. China.
Oncol Lett. 2020 Dec;20(6):323. doi: 10.3892/ol.2020.12186. Epub 2020 Oct 5.
Numerous studies have reported that the long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6; ENSG00000245910) participates in the development of malignant tumors. However, the underlying mechanism of SNHG6 in the development of melanoma remains unknown. Thus, the present study aimed to investigate the biological role of SNHG6 in the progression of melanoma. SNHG6 expression in melanoma tissues and cells was assessed using a bioinformatics approach and reverse transcription-quantitative PCR analysis. Cell viability was determined using the Cell Counting Kit-8 and colony formation assays. The correlation between microRNA (miR)-101-3p, SNHG6 and RAP2B expression levels was assessed using Pearson's correlation analysis. Bioinformatic analysis and luciferase reporter assay were utilized to confirm the interaction between miR-101-3p and SNHG6 or RAP2B. The Transwell assay was conducted to examine the migratory and invasive activities of melanoma cells. In the present study, SNHG6 expression was upregulated in melanoma tissues and cell lines, and SNHG6 silencing suppressed melanoma cell viability, migration and invasion. SNHG6 was directly bound to miR-101-3p, which interacted with RAP2B. In addition, miR-101-3p expression was negatively correlated with SNHG6 or RAP2B expression. miR-101-3p silencing partially abrogated the suppressive effect of SNHG6-knockdown on RAP2B expression. Moreover, the data demonstrated that RAP2B overexpression reversed the inhibitory effects on melanoma cell proliferation, migration and invasion induced by SNHG6 silencing. In conclusion, the present study identified that SNHG6 accelerated melanoma progression via regulating the miR-101-3p/RAP2B axis. Thus, the SNHG6/miR-101-3p/RAP2B signaling pathway may be a novel therapeutic target for melanoma.
大量研究报道，长链非编码RNA（lncRNA）小核仁RNA宿主基因6（SNHG6；ENSG00000245910）参与恶性肿瘤的发生发展。然而，SNHG6在黑色素瘤发生发展中的潜在机制仍不清楚。因此，本研究旨在探讨SNHG6在黑色素瘤进展中的生物学作用。采用生物信息学方法和逆转录-定量PCR分析评估黑色素瘤组织和细胞中SNHG6的表达。使用细胞计数试剂盒-8和集落形成试验测定细胞活力。采用Pearson相关分析评估微小RNA（miR）-101-3p、SNHG6和RAP2B表达水平之间的相关性。利用生物信息学分析和荧光素酶报告基因试验证实miR-101-3p与SNHG6或RAP2B之间的相互作用。进行Transwell试验以检测黑色素瘤细胞的迁移和侵袭活性。在本研究中，黑色素瘤组织和细胞系中SNHG6表达上调，SNHG6沉默抑制黑色素瘤细胞活力、迁移和侵袭。SNHG6直接与miR-101-3p结合，miR-101-3p与RAP2B相互作用。此外，miR-101-3p表达与SNHG6或RAP2B表达呈负相关。miR-101-3p沉默部分消除了SNHG6敲低对RAP2B表达的抑制作用。此外，数据表明RAP2B过表达逆转了SNHG6沉默对黑色素瘤细胞增殖、迁移和侵袭的抑制作用。总之，本研究发现SNHG6通过调节miR-101-3p/RAP2B轴加速黑色素瘤进展。因此，SNHG6/miR-101-3p/RAP2B信号通路可能是黑色素瘤的一个新的治疗靶点。
