LncRNA SNHG16调节miR-212-3p/FAM3C轴对食管癌细胞增殖迁移和侵袭的影响

Effects of LncRNA SNHG16 on the Proliferation Migration and Invasion of Esophageal Cancer Cells via the miR-212-3p/FAM3C Axis

目的:探讨长链非编码小核仁RNA宿主基因16(LncRNA SNHG16)靶向微小RNA-212-3p(miR-212-3p)/序列相似家族3成员C(FAM3C)轴对食管癌细胞增殖、迁移和侵袭的影响。方法:体外培养人食管癌细胞KYSE-510作为研究对象,将其分为对照组、si-NC组、si-SNHG16组、si-SNHG16+inhibitor NC组、si-SNHG16+miR-212-3p inhibitor组。各组细胞LncRNA SNHG16,miR-212-3p、FAM3C mRNA表达的检测用RT-qPCR法;用CCK-8试剂盒检测KYSE-510细胞增殖,用流式细胞术检测KYSE-510细胞凋亡,用划痕实验检测KYSE-510细胞迁移,用Transwell法检测KYSE-510细胞侵袭,双荧光素酶报告实验验证LncRNA SNHG16与miR-212-3p及miR-212-3p与FAM3C之间的靶向关系。结果:与对照组和si-NC组相比,si-SNHG16组中LncRNA SNHG16、FAM3C mRNA水平、OD值、划痕愈合率、细胞侵袭数降低,miR-212-3p水平、细胞凋亡率升高(P<0.05);与si-SNHG16+inhibitor NC组相比,si-SNHG16+miR-212-3p inhibitor组中miR-212-3p水平、细胞凋亡率降低、FAM3C mRNA水平、OD值、划痕愈合率、细胞侵袭数升高(P<0.05),而LncRNA SNHG16水平无差异(P>0.05);生物学信息网站预测miR-212-3p与LncRNA SNHG16和FAM3C均存在靶向结合位,且双荧光素酶报告基因实验验证了LncRNA SNHG16与miR-212-3p、miR-212-3p与FAM3C之间均存在靶向关系(P<0.05)。结论:在食管癌中LncRNA SNHG16表达上调,敲低LncRNA SNHG16的表达可靶向上调miR-212-3p,抑制FAM3C的表达,进而抑制食管癌细胞增殖、迁移和侵袭,促进食管癌细胞的凋亡。

Objective:To investigate the effect of long non-coding small nucleolar RNA host gene 16(LncRNA SNHG16)targeting microRNA-212-3p(miR-212-3p)/Family with sequence similarity 3 member C(FAM3C)axis on the proliferation,migration,and invasion of esophageal cancer cells.Methods:Human esophageal cancer cells KYSE-510 were cultured in vitro and divided into five groups:control group,si-NC group,si-SNHG16 group,si-SNHG16+inhibitor NC group,and si-SNHG16+miR-212-3p inhibitor group.The expression levels of LncRNA SNHG16,miR-212-3p,and FAM3C mRNA were detected using RT-qPCR.The proliferation of KYSE-510 cells was assessed using the CCK-8 assay,apoptosis was analyzed by flow cytometry,migration was evaluated by wound healing assay,and invasion was measured by Transwell assay.The dual-luciferase reporter assay was used to verify the targeting relationship between LncRNA SNHG16 and miR-212-3p,as well as between miR-212-3p and FAM3C.Results:Compared with the control and si-NC groups,the si-SNHG16 group showed decreased levels of LncRNA SNHG16 and FAM3C mRNA,reduced OD values,lower wound healing rates,decreased invasion numbers,and increased miR-212-3p levels and apoptosis rates(P<0.05).Compared with the si-SNHG16+inhibitor NC group,the si-SNHG16+miR-212-3p inhibitor group showed decreased miR-212-3p levels and apoptosis rates,and increased FAM3C mRNA levels,OD values,wound healing rates,and invasion numbers(P<0.05),with no difference in LncRNA SNHG16 levels(P>0.05).Bioinformatics prediction revealed the presence of target binding sites between miR-212-3p and both LncRNA SNHG16 and FAM3C,which was further validated by the dual-luciferase reporter assay(P<0.05).Conclusion:LncRNA SNHG16 is upregulated in esophageal cancer.Knockdown of LncRNA SNHG16 can target and upregulate miR-212-3p,inhibiting the expression of FAM3C,thereby suppressing the proliferation,migration,and invasion of esophageal cancer cells and promoting apoptosis.