[lncRNA DHRS4-AS1通过调节miR-221-3p/SOCS3信号轴对甲状腺癌细胞增殖、侵袭、迁移和凋亡的影响]。

细胞与分子免疫学杂志 Pub Date : 2025-09-01

Hui Wang, Yu Guo, Peipei Zhang, Haoyu Yang, Chuntao Tian, Mingming Jin

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Dual luciferase reporter assays were applied to verify the targeting interaction between lncRNA DHRS4-AS1, SOCS3, and miR-221-3p. Western blot analysis was used to detect the expression of SOCS3 in FTC-133 cells. EdU method was used to measure cell proliferation. Flow cytometry was applied to measure the apoptosis of FTC-133 cells. Scratch experiment was applied to measure the migration of FTC-133 cells. Transwell chamber was applied to detect the invasion of FTC-133 cells. Nude mouse transplantation tumor experiment was used to observe the effect of lncRNA DHRS4-AS1 on the growth of TC transplantation tumors. Results Dual luciferase reporter assays showed a targeting relationship between lncRNA DHRS4-AS1, miR-221-3p, and SOCS3. LncRNA DHRS4-AS1 and SOCS3 were downregulated and miR-221-3p was upregulated in FTC-133 cells. Overexpression of lncRNA DHRS4-AS1 inhibited proliferation, migration, and invasion of FTC-133 cells, while inducing apoptosis. Conversely, miR-221-3p overexpression reversed these inhibitory effects, and suppressed the apoptosis. Nude mouse transplantation experiment observed that overexpression of lncRNA DHRS4-AS1 resulted in a decrease in tumor tissue quality and volume, and a decrease in miR-221-3p expression and an increase in SOCS3 expression. Conclusion LncRNA DHRS4-AS1 is downregulated in FTC-133 cells. 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Methods Quantitative real-time PCR (qRT-PCR) was applied to detect the expression of lncRNA DHRS4-AS1, miR-221-3p, and SOCS3 mRNA in TC cell lines, and the optimal cell line was selected for subsequent experiments. FTC-133 cells were divided into five groups: control group, pcDNA-NC group, DHRS4-AS1 group, DHRS4-AS1 combined with agomir NC group, and DHRS4-AS1 combined with miR-221-3p-agomir group. Transfection efficiency was assessed using qRT-PCR. Dual luciferase reporter assays were applied to verify the targeting interaction between lncRNA DHRS4-AS1, SOCS3, and miR-221-3p. Western blot analysis was used to detect the expression of SOCS3 in FTC-133 cells. EdU method was used to measure cell proliferation. Flow cytometry was applied to measure the apoptosis of FTC-133 cells. Scratch experiment was applied to measure the migration of FTC-133 cells. Transwell chamber was applied to detect the invasion of FTC-133 cells. Nude mouse transplantation tumor experiment was used to observe the effect of lncRNA DHRS4-AS1 on the growth of TC transplantation tumors. Results Dual luciferase reporter assays showed a targeting relationship between lncRNA DHRS4-AS1, miR-221-3p, and SOCS3. LncRNA DHRS4-AS1 and SOCS3 were downregulated and miR-221-3p was upregulated in FTC-133 cells. Overexpression of lncRNA DHRS4-AS1 inhibited proliferation, migration, and invasion of FTC-133 cells, while inducing apoptosis. Conversely, miR-221-3p overexpression reversed these inhibitory effects, and suppressed the apoptosis. Nude mouse transplantation experiment observed that overexpression of lncRNA DHRS4-AS1 resulted in a decrease in tumor tissue quality and volume, and a decrease in miR-221-3p expression and an increase in SOCS3 expression. Conclusion LncRNA DHRS4-AS1 is downregulated in FTC-133 cells. 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引用次数: 0

摘要

目的探讨长链非编码RNA DHRS4-AS1 （lncRNA DHRS4-AS1）通过调控microRNA-221-3p (miR-221-3p)/细胞因子信号传导3 （SOCS3）信号轴对甲状腺癌（TC）细胞增殖、侵袭、迁移及凋亡的影响。方法采用实时荧光定量PCR （Quantitative real-time PCR, qRT-PCR）检测TC细胞株中lncRNA DHRS4-AS1、miR-221-3p和SOCS3 mRNA的表达，选择最佳细胞株进行后续实验。将FTC-133细胞分为5组：对照组、pcDNA-NC组、DHRS4-AS1组、DHRS4-AS1联合agomir NC组、DHRS4-AS1联合miR-221-3p-agomir组。采用qRT-PCR评价转染效率。采用双荧光素酶报告基因检测来验证lncRNA DHRS4-AS1、SOCS3和miR-221-3p之间的靶向相互作用。Western blot检测FTC-133细胞中SOCS3的表达。EdU法测定细胞增殖。流式细胞术检测FTC-133细胞凋亡情况。采用划痕实验检测FTC-133细胞的迁移情况。Transwell室检测FTC-133细胞的侵袭情况。采用裸鼠移植肿瘤实验，观察lncRNA DHRS4-AS1对TC移植肿瘤生长的影响。结果双荧光素酶报告基因检测显示lncRNA DHRS4-AS1、miR-221-3p和SOCS3之间存在靶向关系。FTC-133细胞中LncRNA DHRS4-AS1和SOCS3下调，miR-221-3p上调。lncRNA DHRS4-AS1过表达抑制FTC-133细胞的增殖、迁移和侵袭，同时诱导凋亡。相反，miR-221-3p过表达逆转了这些抑制作用，抑制了细胞凋亡。裸鼠移植实验发现，lncRNA DHRS4-AS1过表达导致肿瘤组织质量和体积下降，miR-221-3p表达降低，SOCS3表达升高。结论LncRNA DHRS4-AS1在FTC-133细胞中表达下调。lncRNA DHRS4-AS1过表达可通过调控miR-221-3p/SOCS3信号轴抑制TC细胞的增殖、侵袭和迁移，诱导凋亡。

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[Effects of lncRNA DHRS4-AS1 on proliferation, invasion, migration, and apoptosis of thyroid cancer cells by regulating the miR-221-3p/SOCS3 signaling axis].

Objective To explore the influences of long-chain noncoding RNA DHRS4-AS1 (lncRNA DHRS4-AS1) on the proliferation, invasion, migration, and apoptosis of thyroid cancer (TC) cells by regulating the microRNA-221-3p (miR-221-3p)/suppressor of cytokine signaling 3 (SOCS3) signaling axis. Methods Quantitative real-time PCR (qRT-PCR) was applied to detect the expression of lncRNA DHRS4-AS1, miR-221-3p, and SOCS3 mRNA in TC cell lines, and the optimal cell line was selected for subsequent experiments. FTC-133 cells were divided into five groups: control group, pcDNA-NC group, DHRS4-AS1 group, DHRS4-AS1 combined with agomir NC group, and DHRS4-AS1 combined with miR-221-3p-agomir group. Transfection efficiency was assessed using qRT-PCR. Dual luciferase reporter assays were applied to verify the targeting interaction between lncRNA DHRS4-AS1, SOCS3, and miR-221-3p. Western blot analysis was used to detect the expression of SOCS3 in FTC-133 cells. EdU method was used to measure cell proliferation. Flow cytometry was applied to measure the apoptosis of FTC-133 cells. Scratch experiment was applied to measure the migration of FTC-133 cells. Transwell chamber was applied to detect the invasion of FTC-133 cells. Nude mouse transplantation tumor experiment was used to observe the effect of lncRNA DHRS4-AS1 on the growth of TC transplantation tumors. Results Dual luciferase reporter assays showed a targeting relationship between lncRNA DHRS4-AS1, miR-221-3p, and SOCS3. LncRNA DHRS4-AS1 and SOCS3 were downregulated and miR-221-3p was upregulated in FTC-133 cells. Overexpression of lncRNA DHRS4-AS1 inhibited proliferation, migration, and invasion of FTC-133 cells, while inducing apoptosis. Conversely, miR-221-3p overexpression reversed these inhibitory effects, and suppressed the apoptosis. Nude mouse transplantation experiment observed that overexpression of lncRNA DHRS4-AS1 resulted in a decrease in tumor tissue quality and volume, and a decrease in miR-221-3p expression and an increase in SOCS3 expression. Conclusion LncRNA DHRS4-AS1 is downregulated in FTC-133 cells. Overexpression of lncRNA DHRS4-AS1 can inhibit the proliferation, invasion, and migration of TC cells and induce apoptosis by regulating the miR-221-3p/SOCS3 signaling axis.

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细胞与分子免疫学杂志

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