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作 者:柳永青 张静 范冬玲 朱加娣 许紫萱 Liu Yongqing;Zhang Jing;Fan Dongling;Zhu Jiadi;Xu Zixuan(Rugao People’s Hospital endocrinology department,Rugao 226500,China;Affiliated Hospital of Nantong University A breast surgery,Nantong 226000,China)
机构地区:[1]如皋市人民医院内分泌科,如皋226500 [2]南通大学附属医院甲乳外科,南通226000
出 处:《中国组织化学与细胞化学杂志》2024年第6期533-539,共7页Chinese Journal of Histochemistry and Cytochemistry
摘 要:目的探讨长链非编码RNA SLC26A4反义RNA1(SLC26A4-AS1)通过调控微小RNA-222-3p(miR-222-3p)抑制甲状腺癌(TC)进展的相关机制。方法Gepia2和db DEMC数据库筛查SLC26A4-AS1、miR-222-3p在TC中的表达;实时荧光定量PCR(q RT-PCR)检测SLC26A4-AS1和miR-222-3p表达;荧光原位杂交(FISH)检测SLC26A4-AS1水平;Ed U染色和Transwell实验检测细胞的增殖、迁移能力;小鼠体内成瘤实验验证SLC26A4-AS1对TC肿瘤生长的影响;Star Base数据库和双荧光素酶报告基因实验预测并验证SLC26A4-AS1、miR-222-3p的靶向关系;免疫荧光法检测丝氨酸/苏氨酸蛋白质激酶4(STK4)蛋白水平。结果在TC细胞中SLC26A4-AS1低表达,miR-222-3p高表达;过表达SLC26A4-AS1可促进STK4表达,并抑制TC细胞的增殖、迁移及小鼠移植瘤的生长;SLC26A4-AS1与miR-222-3p存在靶向关系;转染miR-222-3p模拟物可逆转过表达SLC26A4-AS1对TC细胞恶性行为的抑制。结论过表达SLC26A4-AS1可能通过靶向结合miR-222-3p实现其下调,从而促进STK4表达,抑制TC恶性进展。Objective To investigate the mechanism by which long non-coding RNA SLC26A4 antisense RNA1(SLC26A4-AS1)regulates microRNA-222-3p(miR-222-3p)to inhibit thyroid cancer(TC)progression.Methods The expression of SLC26A4-AS1 and miR-222-3p in TC was screened using the Gepia2 and dbDEMC databases;the expression levels of SLC26A4-AS1 and miR-222-3p were measured by quantitative real-time PCR(qRT-PCR);fluorescence in situ hybridization(FISH)was used to detect the level of SLC26A4-AS1;EdU staining and Transwell assays were performed to assess cell proliferation and migration;tumorigenesis in mice was used to verify the effect of SLC26A4-AS1 on TC tumor growth;the StarBase database and dual-luciferase reporter assay were applied to predict and validate the targeting relationship between SLC26A4-AS1 and miR-222-3p;immunofluorescence was used to detect the level of Ser/Thr protein kinase 4(STK4)protein.Results In TC cells,SLC26A4-AS1 was expressed at low levels,while miR-222-3p was expressed at high levels.Overexpression of SLC26A4-AS1 promoted STK4 expression and inhibited TC cell proliferation,migration,and tumor growth in mice.SLC26A4-AS1 was found to target miR-222-3p.Transfection with miR-222-3p mimic reversed the inhibitory effect of SLC26A4-AS1 overexpression on the malignant behavior of TC cells.Conclusion Overexpression of SLC26A4-AS1 may inhibit TC progression by binding to and downregulating miR-222-3p,thereby promoting STK4 expression.
关 键 词:长链非编码RNA 丝氨酸/苏氨酸蛋白质激酶4 miR-222-3p 甲状腺癌 增殖 迁移
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