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

doi:10.3969/j.issn.1006-6233.2024.08.02

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摘要 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。

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关键词 ：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

Abstract：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.

Key words： Long non-coding small nucleolar RNA host gene 16 microRNA-212-3p/Family with sequence similarity 3 member C Esophageal cancer Proliferation Migration Invasion

基金资助:河北省医学科学研究课题计划,(编号:20240584)

通讯作者: 殷星

引用本文:

侯英利, 冯晓娜, 李春晖, 张萌, 董海平, 殷星. 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[J]. 河北医学, 2024, 30(8): 1238-1244.
HOU Yingli, FENG Xiaona, LI Chunhui, et al. Effects of LncRNA SNHG16 on the Proliferation Migration and Invasion of Esophageal Cancer Cells via the miR-212-3p/FAM3C Axis. HeBei Med, 2024, 30(8): 1238-1244.

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http://www.hbyxzzs.cn/CN/10.3969/j.issn.1006-6233.2024.08.02 或 http://www.hbyxzzs.cn/CN/Y2024/V30/I8/1238

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