Molecular mechanism of miR-19b-3p regulating apoptosis of medullary thyroid cancer cells by targeting<em>MTUS</em>1

陈　国; 韩鹏黎; 陈柯茹; 李明闯; 张青松; 陈　征; 董汉华; 钱跃军; 吕　晶

doi:10.19401/j.cnki.1007-3639.2021.05.005

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Molecular mechanism of miR-19b-3p regulating apoptosis of medullary thyroid cancer cells by targetingMTUS1

更新时间：2026-01-27

- Molecular mechanism of miR-19b-3p regulating apoptosis of medullary thyroid cancer cells by targetingMTUS1
- China Oncology Vol. 31, Issue 5, Pages: 390-396(2021)
- 作者机构：
  
  1. 郑州大学附属郑州中心医院甲状腺外科,河南,郑州,450007
  2. 郑州大学附属郑州中心医院转化医学中心,河南,郑州,450007
- 作者简介：
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2021.05.005
  CLC： R736.1
- Published Online：31 May 2021，
  
  Published：31 May 2021
- 稿件说明：
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陈　国, 韩鹏黎, 陈柯茹, 李明闯, 张青松, 陈　征, 董汉华, 钱跃军, 吕　晶 . miR-19b-3p靶向

陈　国, 韩鹏黎, 陈柯茹, et al. Molecular mechanism of miR-19b-3p regulating apoptosis of medullary thyroid cancer cells by targetingMTUS1[J]. China Oncology, 2021, 31(5): 390-396.
陈　国, 韩鹏黎, 陈柯茹, 李明闯, 张青松, 陈　征, 董汉华, 钱跃军, 吕　晶 . miR-19b-3p靶向 DOI： 10.19401/j.cnki.1007-3639.2021.05.005.

陈　国, 韩鹏黎, 陈柯茹, et al. Molecular mechanism of miR-19b-3p regulating apoptosis of medullary thyroid cancer cells by targetingMTUS1[J]. China Oncology, 2021, 31(5): 390-396. DOI： 10.19401/j.cnki.1007-3639.2021.05.005.

摘要

背景与目的：miR-19b-3p在胃癌、前列腺癌等恶性肿瘤中均呈高表达，其可能作为肿瘤早期诊断及评估患者预后的潜在生物标志物。利用TargetScan靶基因预测软件筛选出的微管相关肿瘤抑制基因1（microtubule-associated tumor suppressor gene 1，MTUS1）可能为miR-19b-3p的靶基因，发现MTUS1的3’非翻译区（3’-untranslated region，3’-UTR）可能是miR-19b-3p的结合位点。探讨miR-19b-3p是否通过靶向MTUS1表达影响甲状腺髓样癌（medullary thyroid cancer，MTC）细胞凋亡。方法：MTC-TT细胞分为anti-miR-19b-3p组、anti-miR-NC组、pcDNA-MTUS1组、pcDNA组、anti-miR-19b-3p+si-MTUS1组、anti-miR-19b-3p+si-NC组、miR-19b-3p组和miR-NC组。采用实时荧光定量聚合酶链反应（real-time fluorescence quantitative polymerase chain reaction，RTFQ-PCR）和蛋白质印迹法（Western blot）分别检测miR-19b-3p和MTUS1的表达水平，采用双荧光素酶报告基因实验验证MTUS1是否为miR-19b-3p的靶基因；采用Western blot检测细胞中Bcl-2、Bax和cleaved caspase-3的表达水平。结果：miR-19b-3p在MTC组织及细胞系中的表达水平显著升高，而MTUS1的表达水平显著降低。转染anti-miR-19b-3p或pcDNA-MTUS1后可显著增强MTC细胞凋亡能力，促进Bax、cleaved caspase-3的表达，抑制Bcl-2的表达。双荧光素酶报告实验证实MTUS1是miR-19b-3p的靶基因。抑制MTUS1表达逆转了抑制miR-19b-3p表达对MTC-TT细胞凋亡的作用。结论：沉默miR-19b-3p表达可上调MTUS1表达从而诱导MTC细胞凋亡。

Abstract

Background and purpose: miR-19b-3p is highly expressed in malignant tumors such as gastric cancer and prostate cancer

which may be used as a potential biomarker for early diagnosis of tumor and evaluation of prognosis of patients. The microtubule-associated tumor suppressor gene 1 (MTUS1) may be miR-19b-3p target gene screened by using TargetScan target gene prediction software

and the 3’-untranslated region (3’-UTR) of MTUS1 may be the binding site of miR-19b-3p. This study aimed to investigate whether miR-19b-3p regulating the expression of MTUS1 and its effect on apoptosis of medullary thyroid cancer (MTC) cells. Methods: MTC-TT cells were divided into anti-miR-19b-3p group

anti-miR-NC group

pcDNA-MTUS1 group

pcDNA group

anti-miR-19b-3p+si-MTUS1 group

anti-miR-19b-3p+si-NC group

miR-19b-3p group and miR-NC group. Expression of miR-19b-3p and MTUS1 were detected by real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) and Western blot. Double luciferase reporter gene assay was performed to confirm whether MTUS1 was the target gene of miR-19b-3p. The expressions of Bcl-2

Bax and cleaved caspase-3 in cells were detected by Western blot. Results: Expression of miR-19b-3p was significantly increased in MTC tissues and cell lines

while the expression level of MTUS1 was significantly decreased. Transfection of anti-miR-19b-3p or pcDNA-MTUS1 significantly promoted the expression of Bax and cleaved caspase-3

while inhibiting Bcl-2 expression. The dual luciferase reporter assay confirmed that MTUS1 was target gene of miR-19b-3p. Inhibition of MTUS1 expression reversed the effect of inhibition of miR-19b-3p expression on apoptosis of MTC-TT cells. Conclusion: Silencing miR-19b-3p can induce apoptosis of MTC TT cells by up-regulating MTUS1 expression.

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Molecular mechanism of miR-19b-3p regulating apoptosis of medullary thyroid cancer cells by targetingMTUS1

DOI：10.19401/j.cnki.1007-3639.2021.05.005

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