Identifying TP53RK as a key regulator of colorectal cancer survival and a potential therapeutic target.

ABSTRACT: Colorectal cancer (CRC) is a leading cause of cancer-related mortality, necessitating the development of novel therapeutic strategies. In the present study, we identified TP53-regulating kinase (TP53RK) as a critical regulator of CRC cell survival and proliferation using a custom clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 library screen targeting serine/threonine kinase-related genes. TP53RK was significantly overexpressed in CRC tissues and was correlated with copy number amplification. Functional validation revealed that TP53RK depletion induced DNA replication stress, apoptosis, and cell cycle arrest, independent from p53 status. Mechanistically, TP53RK stabilized cell division cycle 7 (CDC7), a key kinase regulating DNA replication or

SUBMITTER: Choi Y 

PROVIDER: S-EPMC12533122 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature