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甲状腺转录因子-1在甲状腺癌细胞中对指导自杀基因表达的甲状腺球蛋白启动子的转录激活作用。

Transcriptional activation of the thyroglobulin promoter directing suicide gene expression by thyroid transcription factor-1 in thyroid cancer cells.

作者信息

Shimura H, Suzuki H, Miyazaki A, Furuya F, Ohta K, Haraguchi K, Endo T, Onaya T

机构信息

Third Department of Internal Medicine, Yamanashi Medical University, Yamanashi 409-3898, Japan.

出版信息

Cancer Res. 2001 May 1;61(9):3640-6.

Abstract

Gene therapy with thyroglobulin (TG) promoter and a prodrug/suicide gene combination may prove useful as a treatment for thyroid carcinoma. However, most poorly differentiated and anaplastic thyroid carcinomas have lost the ability to express the TG gene expression accompanied by loss of transcription factors [thyroid transcription factor-1 (TTF-1), TTF-2, or Pax-8] interacting with the TG promoter. In anticipation of developing transcriptionally targeted gene therapy of TG-nonproducing thyroid carcinomas, we investigated the effect of TTF-1 gene transfer on TG promoter activity and the cytotoxic effect obtained by the TG promoter-driven HSV-TK gene along with ganciclovir in thyroid carcinoma and nonthyroidal cells. Using a chimeric construct containing the 5'-flanking region of the rat TG gene between -826 and +39 bp and the luciferase gene, TG promoter activity was detected in a normal rat thyroid cell line (FRTL-5), but not in a dedifferentiated line of thyroid cells (FRT) expressing Pax-8 but not TTF-1, TTF-2, or TG [TTF-1(-)/TTF-2(-)/Pax-8(+)/TG(-)], or in a human papillary thyroid carcinoma cell line [BHP15-3; TTF-1(-)/TTF-2(-)/Pax-8(-)/TG(-)], a human pulmonary cell line [H441; TTF-1(+)/TTF-2(-)/Pax-8(-)/TG(-)], or a dog kidney epithelial cell line [MDCK; TTF-1(-)/TTF-2(-)/Pax-8(+)/TG(-)]. Cotransfection of the TTF-1 expression vector stimulated TG promoter activity in FRT and BHP15-3 dedifferentiated thyroid cells, but not in H441 pulmonary cells. Only weak activation was observed in MDCK kidney cells. We then constructed recombinant adenovirus vectors, AdTTF-1 and ADTGTK: AdTTF-1 contained cytomegalovirus promoter and rat TTF-1 cDNA; AdTGTK carried the TG promoter-driven HSV-TK gene. Infection with AdTGTK and combined with GCV treatment induced a cytotoxic effect in FRTL-5 cells but not in dedifferentiated thyroid or nonthyroid cells. Cotransduction of AdTTF-1 and AdTGTK permitted 90% cytotoxicity for BHP15-3 and >95% cytotoxicity for FRT, as well as for BHP7-13 and BHP18-21v thyroid cancer cell lines [both/TTF1(-)/TTF-2(-)/Pax-8(+)/TG(-)]. In contrast, little cytotoxicity was seen for H441 and MDCK cell lines even with 300 microg/ml of ganciclovir. These results suggest that cotransduction of a TG promoter-controlled suicide gene and the TTF-1 gene by adenoviral vectors confers transcriptionally targeted gene-mediated cytotoxicity in poorly differentiated thyroid carcinoma cells unable to express the TG gene.

摘要

采用甲状腺球蛋白(TG)启动子与前体药物/自杀基因组合进行基因治疗,可能是一种治疗甲状腺癌的有效方法。然而,大多数低分化和未分化甲状腺癌已丧失表达TG基因的能力,同时与TG启动子相互作用的转录因子(甲状腺转录因子-1(TTF-1)、TTF-2或Pax-8)也会缺失。为了开发针对不产生TG的甲状腺癌的转录靶向基因治疗方法,我们研究了TTF-1基因转移对TG启动子活性的影响,以及TG启动子驱动的单纯疱疹病毒胸苷激酶(HSV-TK)基因与更昔洛韦联合使用在甲状腺癌细胞和非甲状腺细胞中产生的细胞毒性作用。使用一种嵌合构建体,其包含大鼠TG基因-826至+39 bp之间的5'侧翼区域和荧光素酶基因,在正常大鼠甲状腺细胞系(FRTL-5)中检测到TG启动子活性,但在表达Pax-8但不表达TTF-1、TTF-2或TG的甲状腺细胞去分化系(FRT)[TTF-1(-)/TTF-2(-)/Pax-8(+)/TG(-)]、人甲状腺乳头状癌细胞系[BHP15-3;TTF-1(-)/TTF-2(-)/Pax-8(-)/TG(-)]、人肺细胞系[H441;TTF-1(+)/TTF-2(-)/Pax-8(-)/TG(-)]或犬肾上皮细胞系[MDCK;TTF-1(-)/TTF-2(-)/Pax-8(+)/TG(-)]中未检测到。将TTF-1表达载体共转染可刺激FRT和BHP15-3去分化甲状腺细胞中的TG启动子活性,但在H441肺细胞中未观察到这种刺激。在MDCK肾细胞中仅观察到微弱的激活。然后,我们构建了重组腺病毒载体AdTTF-1和AdTGTK:AdTTF-1包含巨细胞病毒启动子和大鼠TTF-1 cDNA;AdTGTK携带TG启动子驱动的HSV-TK基因。用AdTGTK感染并联合GCV处理在FRTL-5细胞中诱导了细胞毒性作用,但在去分化甲状腺细胞或非甲状腺细胞中未诱导。AdTTF-1和AdTGTK的共转导对BHP15-3细胞产生了90%的细胞毒性,对FRT以及BHP7-13和BHP18-21v甲状腺癌细胞系[两者均为/TTF1(-)/TTF-2(-)/Pax-8(+)/TG(-)]产生了>95%的细胞毒性。相比之下,即使使用300μg/ml的更昔洛韦,H441和MDCK细胞系中也几乎没有观察到细胞毒性。这些结果表明,腺病毒载体共转导TG启动子控制的自杀基因和TTF-1基因,可在无法表达TG基因的低分化甲状腺癌细胞中赋予转录靶向基因介导的细胞毒性。

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