PDF(Pubmed)
Abstract：
Anaplastic thyroid carcinoma (ATC) is an extremely aggressive tumor with a high mortality rate and poor prognosis. However, the pathogenesis of ATC is complex and poorly understood, and the effective treatment options are limited. Analysis of data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases showed that collagen triple helix repeat containing-1 (CTHRC1) was specifically upregulated in ATC tissues and was negatively correlated with overall survival (OS) in thyroid carcinoma patients. In vitro knockdown of CTHRC1 dramatically decreased the proliferation, migration, and invasion abilities of ATC cells, and in vivo studies in BALB/c nude mice confirmed that CTHRC1 knockdown significantly inhibited tumor growth. Mechanistically, CTHRC1 knockdown was found to suppress the Wnt/β-catenin pathway and epithelial-mesenchymal transition (EMT) at the protein level. These findings suggest that CTHRC1 promotes the progression of ATC via upregulating tumor cell proliferation, migration, and invasion, which may be achieved by activating the Wnt/β-catenin pathway and EMT.
摘要：
间变性甲状腺癌（ATC）是一种侵袭性极强的肿瘤，死亡率高，预后差。然而,ATC的发病机制复杂且知之甚少，有效的治疗方案是有限的。对来自基因表达综合（GEO）和癌症基因组图谱（TCGA）数据库的数据进行的分析显示，含胶原蛋白三螺旋重复序列1（CTHRC1）在ATC组织中被特异性上调，并且与总体生存率（OS）呈负相关。甲状腺癌患者。在体外敲低CTHRC1显著降低增殖，迁移,以及ATC细胞的侵袭能力,BALB/c裸鼠体内研究证实CTHRC1敲低可显著抑制肿瘤生长。机械上,发现CTHRC1敲低在蛋白质水平上抑制Wnt/β-catenin途径和上皮-间质转化（EMT）。这些发现表明，CTHRC1通过上调肿瘤细胞增殖促进ATC的进展，迁移,和入侵,这可以通过激活Wnt/β-连环蛋白途径和EMT来实现。
