DDA1, also known as DET1 and DDB1 associated 1, is an evolutionarily conserved gene. It is involved in multiple important biological functions. It has been linked to the ubiquitin-proteasome pathway, and is an integral component of the CRL4CSA ubiquitin ligase complex, regulating transcription-coupled nucleotide excision repair (TC-NER) dynamics [2,3]. It is also associated with several signaling pathways like STAT3, NFκB/CSN2/GSK-3β, and may play a role in cell cycle regulation [1,4].

In breast cancer, DDA1 and p-STAT3 levels are elevated in cisplatin-resistant cells. DHA treatment represses cell proliferation and induces apoptosis by suppressing STAT3 phosphorylation, and DDA1 knockdown inhibits cyclin expression, promotes cell cycle arrest, and induces apoptosis of resistant cells [1]. In stage IIB-IIC colon cancer, DDA1 promotes tumor progression by activating the NFκB/CSN2/GSK-3β signaling pathway, and its overexpression in colon cancer lines promotes cell proliferation, cell cycle progression, and invasion [4]. In lung cancer, DDA1 overexpression promotes proliferation of lung tumour cells and tumour progression in vivo, potentially through promoting cyclins and cell cycle progression [5].

In conclusion, DDA1 plays crucial roles in various biological processes such as DNA repair, cell cycle regulation, and in multiple cancer-related disease conditions like breast, colon, and lung cancers. Understanding DDA1's functions through studies, including potential gene knockout models, could provide new insights into cancer development mechanisms and potential therapeutic targets.