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低水平的金属硫蛋白1M(MT1M)与甲状腺癌细胞系的进展相关。

Low metallothionein 1M (MT1M) is associated with thyroid cancer cell lines progression.

作者信息

Chen Yizuo, Quan Ruida, Bhandari Adheesh, Chen Zheng, Guan Yaoyao, Xiang Jingjing, You Jie, Teng Lisong

机构信息

The First Affiliated Hospital, College of Medicine, Zhejiang University Hangzhou, Zhejiang, People's Republic of China.

Department of Thyroid and Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University Wenzhou, Zhejiang, People's Republic of China.

出版信息

Am J Transl Res. 2019 Mar 15;11(3):1760-1770. eCollection 2019.

PMID:30972199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6456523/
Abstract

Papillary thyroid cancer (PTC) is the most common malignancy of the thyroid carcinoma, despite ongoing advances, novel biomarkers are required for prognosis and diagnosis of PTC. Our previous research found that metallothionein 1M (MT1M) was a novel potential PTC associated gene in thyroid cancer. In the present study, the expression status and prognostic value of MT1M expression were investigated in thyroid cancer. Tissue samples from 60 patients with PTC were subjected to the quantitative real-time polymerase chain reaction and the relative expression of MT1M in the patient tissue was evaluated. The Cancer Genome Atlas (TCGA) RNA-seq database was downloaded to further explore the role of MT1M in PTC and its relationship with lymph node metastasis (LNM). Logistic analysis showed that reduced expression of MT1M, histological type, and clinical stage are independent high-risk factors for LNM in PTC. The biological function of MT1M was also researched by using the PTC cell lines TPC-1, KTC1 and BCPAP. In vitro experiments revealed that MT1M upregulation significantly inhibits the colony formation, proliferation, migration, and invasion of PTC cell lines. We also found that MT1M could modulate the expression of N-cadherin and vimentin. These results implied that MT1M involved in the progress of thyroid cancer and might act as a tumor suppressor gene. In this study, we identified, for the first time, MT1M was involved in thyroid carcinoma cell lines This study specified a potential new marker and a target for gene therapy in thyroid cancer treatment.

摘要

甲状腺乳头状癌(PTC)是甲状腺癌中最常见的恶性肿瘤,尽管医学不断进步,但仍需要新的生物标志物用于PTC的预后评估和诊断。我们之前的研究发现,金属硫蛋白1M(MT1M)是甲状腺癌中一个新的潜在PTC相关基因。在本研究中,我们调查了MT1M在甲状腺癌中的表达状态及其预后价值。对60例PTC患者的组织样本进行了定量实时聚合酶链反应,并评估了患者组织中MT1M的相对表达。下载癌症基因组图谱(TCGA)RNA测序数据库以进一步探究MT1M在PTC中的作用及其与淋巴结转移(LNM)的关系。逻辑分析表明,MT1M表达降低、组织学类型和临床分期是PTC患者发生LNM的独立高危因素。还利用PTC细胞系TPC-1、KTC1和BCPAP研究了MT1M的生物学功能。体外实验表明,MT1M上调可显著抑制PTC细胞系的集落形成、增殖、迁移和侵袭。我们还发现MT1M可调节N-钙黏蛋白和波形蛋白的表达。这些结果表明MT1M参与了甲状腺癌的进展,可能作为一种肿瘤抑制基因发挥作用。在本研究中,我们首次发现MT1M参与甲状腺癌细胞系。本研究明确了甲状腺癌治疗中一个潜在的新标志物和基因治疗靶点。

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