ADCK1 activates the β-catenin/TCF signaling pathway to promote the growth and migration of colon cancer cells

As a result of mutations in the upstream components of the Wnt/beta -catenin signaling pathway, this cascade is abnormally activated in colon cancer. Hence, identifying the activation mechanism of this pathway is an urgent need for the treatment of colon cancer. Here, we found an increase in ADCK1 (AarF domain-containing kinase 1) expression in clinical specimens of colon cancer and animal models. Upregulation of ADCK1 expression promoted the colony formation and infiltration of cancer cells. Downregulation of ADCK1 expression inhibited the colony formation and infiltration of cancer cells, in vivo tumorigenesis, migration, and organoid formation. Molecular mechanistic studies demonstrated that ADCK1 interacted with TCF4 (T-cell factor 4) to activate the beta -catenin/TCF signaling pathway. In conclusion, our research revealed the functions of ADCK1 in the development of colon cancer and provided potential therapeutic targets.

Automated summary

Mutations in the Wnt/beta-catenin signaling pathway upstream lead to abnormal activation in colon cancer, and ADCK1 plays a crucial role in promoting cancer progression by interacting with TCF4 to activate the beta-catenin/TCF pathway. This research identifies potential therapeutic targets for colon cancer treatment.