BCL7B, a member of the B-cell lymphoma 7 protein family, is an accessory subunit of the SWI/SNF chromatin-remodelling complex. It participates in multiple biological processes, influencing gene expression by regulating chromatin structure. It is associated with pathways like the Wnt-signaling pathway and apoptotic pathway, and is of great significance in cancer-related research [3,5].

In cancer studies, heterozygous BCL7B-deficient stomach cancer cell lines generated via Nuclease technology showed downregulation of immune-related genes and upregulation of stemness-related genes. ChIP-seq analysis also revealed changes in epigenetic modification sequences, affecting antigen presentation. These changes led to cancer stem cell-like characteristics and immune evasion in cancer cells [1]. In pancreatic cancer, high BCL7B expression was an independent predictor of poor prognosis, and knockdown of BCL7B inhibited cell motility and invasion through influencing CREB signaling [4]. In sarcomas, BCL7B was a potential biomarker for diagnosis and prognosis, and its low expression was associated with poor overall survival. Gene set enrichment analysis showed differential enrichment of certain pathways in BCL7B low-expression phenotypes [2].

In conclusion, BCL7B, as a subunit of the SWI/SNF complex, plays a crucial role in regulating gene expression related to cancer immunity and stemness. Its dysregulation is associated with poor prognosis in various cancers, such as pancreatic cancer and sarcomas. Studies using gene-knockout models in cancer cells have provided important insights into the functions of BCL7B in cancer development and progression.