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RET/PTC1 与 TTF1 的同时过表达赋予甲状腺细胞致瘤性。

Concurrent overexpression of RET/PTC1 and TTF1 confers tumorigenicity to thyrocytes.

机构信息

Third Department of Internal Medicine, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo City, Yamanashi 409-3898, Japan.

出版信息

Endocr Relat Cancer. 2013 Oct 14;20(6):767-76. doi: 10.1530/ERC-13-0310. Print 2013 Dec.

DOI:10.1530/ERC-13-0310
PMID:24014739
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3796879/
Abstract

A variant located on 14q13.3 nearest to thyroid transcription factor-1 (TTF1) predisposes individuals to thyroid cancer, but whether this variant is related to the RET/PTC rearrangement associated with human papillary thyroid carcinomas (PTCs) is unknown. The aims of this study were to investigate the effects of RET/PTC1 on the expression of thyroid-specific genes in thyrocytes and their relationship with malignant transformation of the thyrocytes. In the absence or presence of TSH, an extracellular signal-regulated kinase was phosphorylated in FRTL5 cells that stably expressed RET/PTC1, and these cells grew independently of TSH. FRTL (RET/PTC1) cells produced 566% more thyroglobulin mRNA and 474% more Na+/I- symporter mRNA than did the control FRTL (pcDNA) cells. FRTL (RET/PTC1) cells expressed 468% more Ttf1 mRNA than did FRTL (pcDNA) cells, but these two cell types did not differ significantly with respect to Pax8 or Ttf2 mRNA levels. When FRTL (RET/PTC1) cells and FRTL (pcDNA), cells were injected into each of nine nude mice, each mouse developed a single tumor at the site of FRTL (RET/PTC1) cell injection; in contrast, tumor formation never occurred at sites of FRTL (cDNA) cells injection. Tumors resulting from FRTL (RET/PTC1) cells retained (125)I-uptake activity; moreover, the cells invaded into surrounding skeletal muscle. When overexpression of Ttf1 in FRTL (RET/PTC1) cells was silenced, the cells completely lost their tumorigenic potential. Exogenous TTF1 cDNA enhanced the tumorigenicity of BHP18-21v cells, human PTC cells that express RET/PTC1, in nude mice. These results indicated that concurrent overexpression of RET/PTC1 and TTF1 confers tumorigenicity to FRTL5 and BHP18-21v cells in nude mice.

摘要

位于 14q13.3 上且紧邻甲状腺转录因子-1（TTF1）的变异体使个体易患甲状腺癌，但该变异体是否与人类甲状腺乳头状癌（PTC）相关的 RET/PTC 重排有关尚不清楚。本研究的目的是研究 RET/PTC1 对甲状腺细胞中甲状腺特异性基因表达的影响及其与甲状腺细胞恶性转化的关系。在存在或不存在 TSH 的情况下，稳定表达 RET/PTC1 的 FRTL5 细胞中的细胞外信号调节激酶被磷酸化，这些细胞可以独立于 TSH 生长。与对照 FRTL（pcDNA）细胞相比，FRTL（RET/PTC1）细胞产生的甲状腺球蛋白 mRNA 多 566%，Na+/I- 同向转运体 mRNA 多 474%。FRTL（RET/PTC1）细胞表达的 Ttf1 mRNA 比 FRTL（pcDNA）细胞多 468%，但这两种细胞类型在 Pax8 或 Ttf2 mRNA 水平上没有显著差异。当将 FRTL（RET/PTC1）细胞和 FRTL（pcDNA）细胞分别注射到 9 只裸鼠中时，每只裸鼠在 FRTL（RET/PTC1）细胞注射部位均形成单个肿瘤；相比之下，FRTL（cDNA）细胞注射部位从未发生肿瘤形成。源自 FRTL（RET/PTC1）细胞的肿瘤保留了（125）I 摄取活性；此外，这些细胞还侵入周围骨骼肌。当 FRTL（RET/PTC1）细胞中的 Ttf1 过表达被沉默时，这些细胞完全失去了其致瘤潜能。外源性 TTF1 cDNA 增强了在裸鼠中表达 RET/PTC1 的 BHP18-21v 细胞的致瘤性。这些结果表明，RET/PTC1 和 TTF1 的同时过表达赋予 FRTL5 和 BHP18-21v 细胞在裸鼠中的致瘤性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71d9/3796879/b87fca9441c5/ERC130310f05.jpg
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