高级搜索
王群, 袁杰, 黄军, 梅虹. 上调LncRNA RP11-173C1.1对甲状腺癌B-CPAP细胞增殖和侵袭能力的影响[J]. 肿瘤防治研究, 2020, 47(3): 170-174. DOI: 10.3971/j.issn.1000-8578.2020.19.0457
引用本文: 王群, 袁杰, 黄军, 梅虹. 上调LncRNA RP11-173C1.1对甲状腺癌B-CPAP细胞增殖和侵袭能力的影响[J]. 肿瘤防治研究, 2020, 47(3): 170-174. DOI: 10.3971/j.issn.1000-8578.2020.19.0457
WANG Qun, YUAN Jie, HUANG Jun, MEI Hong. Effect of LncRNA RP11-173C1.1 Overexpression on Proliferation and Invasion of Thyroid Carcinoma B-CPAP Cells[J]. Cancer Research on Prevention and Treatment, 2020, 47(3): 170-174. DOI: 10.3971/j.issn.1000-8578.2020.19.0457
Citation: WANG Qun, YUAN Jie, HUANG Jun, MEI Hong. Effect of LncRNA RP11-173C1.1 Overexpression on Proliferation and Invasion of Thyroid Carcinoma B-CPAP Cells[J]. Cancer Research on Prevention and Treatment, 2020, 47(3): 170-174. DOI: 10.3971/j.issn.1000-8578.2020.19.0457

上调LncRNA RP11-173C1.1对甲状腺癌B-CPAP细胞增殖和侵袭能力的影响

Effect of LncRNA RP11-173C1.1 Overexpression on Proliferation and Invasion of Thyroid Carcinoma B-CPAP Cells

  • 摘要:
    目的 检测长链非编码RNA RP11-173C1.1在分化型甲状腺癌组织中的表达,并研究RP11-173C1.1对甲状腺乳头状癌细胞系B-CPAP增殖和侵袭的作用和分子机制。
    方法 qRT-PCR检测分化型甲状腺癌组织、甲状腺癌细胞株中RP11-173C1.1的表达。以表达水平最低的B-CPAP细胞为研究对象,转染RP11-173C1.1过表达质粒和阴性对照质粒,分别命名为实验组和对照组。CCK-8法、Transwell侵袭实验分别检测上调RP11-173C1.1对B-CPAP细胞增殖和侵袭能力的影响。生物信息学方法预测RP11-173C1.1的作用机制。qRT-PCR和Western blot检测上调RP11-173C1.1对下游基因表达的影响。
    结果 甲状腺癌组织中RP11-173C1.1的表达显著低于癌旁组织(P < 0.01)。甲状腺癌细胞株中RP11-173C1.1的表达显著低于正常甲状腺滤泡上皮细胞(P < 0.01)。上调RP11-173C1.1可抑制B-CPAP细胞的增殖和侵袭能力(均P < 0.05)。RP11-173C1.1互补结合miR-376c-3p,miR-376c-3p互补结合OPCML。上调RP11-173C1.1可降低B-CPAP细胞中miR-376c-3p的表达,促进OPCML mRNA和蛋白的表达(均P < 0.01)。
    结论 RP11-173C1.1在分化型甲状腺癌组织和细胞系中呈低表达,上调RP11-173C1.1可抑制甲状腺乳头状癌细胞系B-CPAP的增殖和侵袭能力,其可能的机制是通过下调miR-376c-3p的表达、上调OPCML基因的表达来实现。

     

    Abstract:
    Objective To detect the expression of lncRNA RP11-173C1.1 in differentiated thyroid tissue, and to investigate the effect of RP11-173C1.1 on the proliferation and invasion of thyroid papillary carcinoma cell line B-CPAP and the molecular mechanism.
    Methods qRT-PCR was used to detect the expression level of RP11-173C1.1 in differentiated thyroid cancer tissues and thyroid cancer cell lines. The B-CPAP cells with the lowest expression level were used as the research object, and the RP11-173C1.1 overexpression plasmid and the negative control plasmid were transfected into the experimental group and the control group, respectively. The effects of RP11-173C1.1 on the proliferation and invasion of B-CPAP cells were detected by CCK-8 and Transwell invasion assays, respectively. The bioinformatics method predicted the mechanism of RP11-173C1.1. qRT-PCR and Western blot were used to detect the effect of RP11-173C1.1 on downstream gene expression.
    Results The expression of RP11-173C1.1 was significantly lower in thyroid cancer tissues than that in adjacent tissues (P < 0.01). The expression of RP11-173C1.1 in thyroid cancer cell lines was significantly lower than that in normal thyroid follicular epithelial cells (P < 0.01). Up-regulation of RP11-173C1.1 inhibited the proliferation and invasion abilities of B-CPAP cells (both P < 0.05). RP11-173C1.1 complemented miR-376c-3p, and miR-376c-3p complemented OPCML. Up-regulation of RP11-173C1.1 reduced miR-376c-3p expression and promoted OPCML mRNA and protein expression in B-CPAP cells (all P < 0.01).
    Conclusion RP11-173C1.1 is lowly expressed in differentiated thyroid carcinoma tissues and cell lines. Up-regulation of RP11-173C1.1 could inhibit the proliferation and invasion of thyroid papillary carcinoma cell line B-CPAP. The possible mechanism is down-regulating miR-376c-3p expression and up-regulating OPCML gene expression.

     

/

返回文章
返回