CTHRC1 promotes anaplastic thyroid cancer progression by upregulating the proliferation, migration, and invasion of tumor cells

PeerJ

article

Yong Chen¹  Lanning Jia¹  Ke Zhao¹  Zuoyu Chen¹  Yue Han¹  Xianghui He¹ 

[1]Department of General Surgery, Tianjin Medical University General Hospital

[2]Department of General Surgery, Huai’an Second People’s Hospital

关键词: Anaplastic thyroid cancer;    CTHRC1;    EMT;    Wnt/β-catenin pathway;   

DOI  :  10.7717/peerj.15458

学科分类：社会科学、人文和艺术（综合）

来源: Inra

【 摘 要 】

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.

【 授权许可】

CC BY