Chd1l, also known as ALC1 (amplified in liver cancer 1), is a multifunctional gene encoding a protein involved in diverse cellular processes. It plays a role in chromosome remodeling, cell differentiation, and development. Chd1l is crucial for chromosomal integrity maintenance, DNA repair, and transcriptional regulation through its DNA-binding ability. By regulating complex networks, it acts as an anti-apoptotic and pro-proliferative factor. It has been identified as an oncoprotein as its overexpression dysregulates downstream targets in various cancers [1,2].

In hepatocellular carcinoma, CHD1L-iKO cell line studies showed that deletion of Chd1l increased the expression of ZKSCAN3, a key autophagy suppressor, impaired autophagic flux and cell migration. This indicates that Chd1l promotes HCC cell migration and metastasis through autophagy by targeting ZKSCAN3 [3]. In osteosarcoma, knockdown of Chd1l reduced cell proliferation, induced apoptosis in cisplatin-resistant cells, decreased the properties of cancer stem cells, and down-regulated MDR-1 expression. It also restrained the activation of ERK1/2, AKT, and NF-κB signaling pathways, mitigating cisplatin resistance in xenografts [4].

In conclusion, Chd1l is a multifunctional gene with important roles in normal cell function and tumorigenesis. Through gene-knockout and conditional-knockout models, its role in promoting tumor cell migration, metastasis, and chemoresistance in cancers like hepatocellular carcinoma and osteosarcoma has been revealed. Understanding Chd1l's functions can potentially lead to new targeted therapeutic strategies for these diseases.