■本研究旨在通过靶向miR-506-3p/ETS原癌基因1,转录因子(ETS1)/RAS/细胞外调节蛋白激酶(ERK)分子轴,探讨长链非编码核糖核酸(lncRNA)SNHG16对肾透明细胞癌(KIRC)细胞的作用机制。从而为今后KIRC的临床诊断和治疗提供参考。
■本研究纳入了36名KIRC患者,取其癌组织及癌旁组织检测SNHG16/miR-506-3p/ETS1/RAS/ERK表达。然后,将过表达的SNHG16质粒和沉默质粒分别转染KIRC细胞,观察其生物学行为的变化。
■SNHG16和ETS1在KIRC组织中高表达,miR-506-3p低表达;RAS/ERK信号通路在KIRC组织中显著激活(P<0.05)。在SNHG16沉默之后,KIRC细胞增殖减少,侵袭和迁移能力和增加的细胞凋亡率;相应地,SNHG16表达的增加获得了相反的结果(P<0.05)。最后,在救援实验中,同时增加miR-506-3p可以逆转SNHG16对KIRC细胞的影响,miR-506-3p的作用被ETS1逆转。RAS/ERK途径的激活与ETS1的增加具有相同的作用,这进一步恶化了KIRC的恶性程度。在miR-506-3p增加和ETS1沉默后,RAS/ERK信号通路受到抑制(P<0.05)。最后,拯救实验(共转染)证实SNHG16对KIRC细胞的作用是通过miR-506-3p/ETS1/RAS/ERK分子轴实现的.
■SNHG16通过靶向miR-506-3p/ETS1/RAS/ERK分子轴调节KIRC细胞的生物学行为。
UNASSIGNED: This study aimed to investigate the mechanism of long noncoding ribonucleic acid (lncRNA) SNHG16 on kidney clear cell carcinoma (KIRC) cells by targeting miR-506-3p/ETS proto-oncogene 1, transcription factor (
ETS1)/RAS/Extracellular regulated protein kinases (ERK) molecular axis, thus to provide reference for clinical diagnosis and treatment of KIRC in the future.
UNASSIGNED: Thirty-six patients with KIRC were enrolled in this study, and their carcinoma tissues and adjacent tissues were obtained for the detection of SNHG16/miR-506-3p/
ETS1/RAS/ERK expression. Then, over-expressed SNHG16 plasmid and silenced plasmid were transfected into KIRC cells to observe the changes of their biological behavior.
UNASSIGNED: SNHG16 and
ETS1 were highly expressed while miR-506- 3p was low expressed in KIRC tissues; the RAS/ERK signaling pathway was significantly activated in KIRC tissues (P < 0.05). After SNHG16 silence, KIRC cells showed decreased proliferation, invasion and migration capabilities and increased apoptosis rate; correspondingly, increase in SNHG16 expression achieved opposite results (P < 0.05). Finally, in the rescue experiment, the effects of elevated SNHG16 on KIRC cells were reversed by simultaneous increase in miR-506-3p, and the effects of miR-506-3p were reversed by ETS1. Activation of the RAS/ERK pathway had the same effect as increase in
ETS1, which further worsened the malignancy of KIRC. After miR-506-3p increase and
ETS1 silence, the RAS/ERK signaling pathway was inhibited (P < 0.05). At last, the rescue experiment (co-transfection) confirmed that the effect of SNHG16 on KIRC cells is achieved via the miR-506-3p/ETS1/RAS/ERK molecular axis.
UNASSIGNED: SNHG16 regulates the biological behavior of KIRC cells by targeting the miR-506-3p/ETS1/RAS/ERK molecular axis.