Description

The DYRK2 Knockout KYSE-150 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from human KYSE-150 esophageal squamous cell carcinoma cells. This loss-of-function model enables targeted disruption of DYRK2, a tumor-suppressive kinase. Generated via CRISPR/Cas9-mediated gene editing, the line provides stable DYRK2 ablation for functional studies in apoptosis, DNA damage response, and Wnt signaling. Supplied as a ready-to-use product, it accelerates research into DYRK2-dependent mechanisms without the need for in-house gene editing.

The parental KYSE-150 line is a poorly differentiated esophageal squamous cell carcinoma model established from a Japanese male. It is widely used to study esophageal cancer pathogenesis, drug responses, and metastasis. The genetic landscape of KYSE-150 reflects typical mutations found in this cancer type, offering a clinically relevant background for examining tumor suppressor gene function. Introducing a DYRK2 knockout into KYSE-150 allows dissection of DYRK2??s role in esophageal carcinoma progression.

DYRK2 is a dual-specificity kinase acting as a tumor suppressor by phosphorylating p53 at Ser46 to drive apoptosis upon DNA damage. Upstream ATM and ATR kinases activate DYRK2, which then modifies p53, inducing pro-apoptotic Bax and Puma and caspase-3 activation. DYRK2 also regulates Wnt signaling by phosphorylating Dvl2 and Dvl3, promoting ??-catenin degradation and inhibiting TCF4-driven transcription of c-Myc and Snail. Interactions with 14-3-3 and MDM2 further fine-tune p53 stability. Thus, DYRK2 integrates DNA damage and Wnt signals to control cell cycle, apoptosis, and EMT.

Loss of DYRK2 in esophageal squamous cell carcinoma compromises p53-mediated apoptosis and enhances survival, contributing to therapy resistance. This knockout line enables investigation of DYRK2 deficiency on genotoxic drug responses (e.g., cisplatin, 5-FU). Comparative analyses with parental cells can clarify DYRK2??s impact on DNA damage checkpoints, apoptotic priming, and Wnt-driven proliferation. The model is valuable for studying crosstalk between p53 and ??-catenin/TCF4 pathways and identifying synthetic lethal targets in DYRK2-null tumors.

This knockout cell line supports diverse assays: apoptosis (Annexin V/PI), cell cycle analysis, viability and drug sensitivity tests, migration/invasion assays for EMT, colony formation, and xenograft studies. It also facilitates RNA-seq and co-immunoprecipitation for mapping DYRK2-driven networks. Phospho-specific detection of p53 Ser46 serves as a kinase activity readout. For further details, contact Ascent Research.