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

PeerJ. 2023 May 29:11:e15458. doi: 10.7717/peerj.15458. eCollection 2023.

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.

Keywords: Anaplastic thyroid cancer; CTHRC1; EMT; Wnt/β-catenin pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Extracellular Matrix Proteins* / genetics
  • Mice
  • Mice, Nude
  • Neoplastic Processes
  • Thyroid Carcinoma, Anaplastic* / genetics
  • Thyroid Neoplasms* / genetics
  • beta Catenin / genetics

Substances

  • beta Catenin
  • Extracellular Matrix Proteins
  • Cthrc1 protein, mouse

Grants and funding

This study was funded by the Tianjin Education Commission Scientific Research Project (2020KJ153). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.