Long non-coding RNA SNHG6 promotes cell proliferation and migration through sponging miR-4465 in ovarian clear cell carcinoma
Long non-coding RNA SNHG6 promotes cell proliferation and migration through sponging miR-4465 in ovarian clear cell carcinoma
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长非编码RNA SNHG6通过海绵miR-4465促进卵巢透明细胞癌细胞增殖和迁移
DOI：
10.1111/jcmm.14359
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发表时间：
2019-08-01
影响因子：
5.3
通讯作者：
Wu, Xiaohua
中科院分区：
文献类型：
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作者：
Wu, Yong;Deng, Yu;Wu, Xiaohua
小核仁RNA宿主基因6 （SNHG6）的失调在人类癌症中发挥关键的致癌作用并促进肿瘤的发生。然而，关于SNHG6在卵巢透明细胞癌（OCCC）中的表达模式的信息很少，并且这种长链非编码RNA在OCCC的肿瘤发生和进展中的作用尚不清楚。在本研究中，我们通过实时荧光定量PCR发现，相对于未配对的正常卵巢组织，SNHG6在OCCC组织中的表达异常上调。SNHG6高表达与血管侵犯、远处转移和生存不良相关。进一步的功能实验表明，在OCCC细胞中，敲低SNHG6可以抑制细胞的体外增殖、迁移和侵袭以及体内肿瘤的生长。此外，SNHG6作为竞争内源性RNA (ceRNA)，有效地充当miR-4465的海绵，从而调节zeste同源物2的增强子（EZH2）的表达。综上所述，我们的数据表明SNHG6是参与OCCC进展的新分子，靶向涉及SNHG6的ceRNA网络可能是OCCC的一种治疗策略。
Dysregulation of small nucleolar RNA host gene 6 (SNHG6) exerts critical oncogenic effects and facilitates tumourigenesis in human cancers. However, little information about the expression pattern of SNHG6 in ovarian clear cell carcinoma (OCCC) is available, and the contributions of this long non-coding RNA to the tumourigenesis and progression of OCCC are unclear. In the present study, we showed via quantitative real-time PCR that SNHG6 expression was abnormally up-regulated in OCCC tissues relative to that in unpaired normal ovarian tissues. High SNHG6 expression was correlated with vascular invasion, distant metastasis and poor survival. Further functional experiments demonstrated that knockdown of SNHG6 in OCCC cells inhibited cell proliferation, migration and invasion in vitro as well as tumour growth in vivo. Moreover, SNHG6 functioned as a competing endogenous RNA (ceRNA), effectively acting as a sponge for miR-4465 and thereby modulating the expression of enhancer of zeste homolog 2 (EZH2). Taken together, our data suggest that SNHG6 is a novel molecule involved in OCCC progression and that targeting the ceRNA network involving SNHG6 may be a treatment strategy in OCCC.