Ddb2, also known as damage-specific DNA-binding protein 2, is initially identified as a DNA damage recognition factor crucial for global genomic nucleotide excision repair (GG-NER) in human cells. It also involves in multiple essential biological processes such as chromatin remodeling, gene transcription, cell cycle regulation, and protein decay [1].

In cancer research, Ddb2 shows diverse roles. In pancreatic ductal adenocarcinoma (PDAC), its reduced expression in cancer tissues is related to shorter disease-free survival. Overexpression of Ddb2 in PDAC cells can repress epithelial-to-mesenchymal transition (EMT), inhibit cell migration and invasion, and sensitize cells to chemotherapy drugs like 5-fluorouracil, oxaliplatin, and gemcitabine, indicating its potential as a tumor suppressor in PDAC [2]. In melanoma, Ddb2 promotes cell growth by transcriptionally regulating the expression of KMT2A, and high Ddb2 levels predict a poor prognosis [3].

In conclusion, Ddb2 is vital for DNA repair and various biological processes. Its role in cancer development, such as in PDAC and melanoma, has been revealed through functional studies. These findings from model-based research on Ddb2 contribute to understanding the mechanisms of cancer development and may provide new therapeutic strategies for related cancers.