首页|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

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

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  • 国家科技期刊平台
  • NETL
  • NSTL
  • 万方数据
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+in-hibitor 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。
Effects of LncRNA SNHG16 on the Proliferation Migration and Invasion of Esophageal Cancer Cells via the miR-212-3p/FAM3C Axis
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 mem-ber C(FAM3C)axis on the proliferation,migration,and invasion of esophageal cancer cells.Methods:Hu-man 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 con-trol and si-NC groups,the si-SNHG16 group showed decreased levels of LncRNA SNHG16 and FAM3C mR-NA,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 in-creased 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 promo-ting apoptosis.

Long non-coding small nucleolar RNA host gene 16microRNA-212-3p/Family with sequence similarity 3 member CEsophageal cancerProliferationMigrationInvasion

侯英利、冯晓娜、李春晖、张萌、董海平、殷星

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河北省邯郸市第一医院肿瘤一科,河北 邯郸 056000

长链非编码小核仁RNA宿主基因16 微小RNA-212-3p/序列相似家族3成员C 食管癌 增殖 迁移 侵袭

河北省医学科学研究课题计划

20240584

2024

10.3969/j.issn.1006-6233.2024.08.02

河北医学
河北省医学会

河北医学

CSTPCD
影响因子：1.915
ISSN：1006-6233
年,卷(期)：2024.30(8)