SpiB, a member of the E-twenty-six (ETS) transcription factor family, is essential for the survival of mature B cells and plays a key role in multiple biological processes. It is involved in regulating B-cell-related genes, autophagy, apoptosis, and cell-cycle arrest, and is associated with pathways such as JAK1/STAT6, NF-κB, and JNK [1,2,4].

In IgG1+ cell-specific SpiB conditional knockout (cKO) mice, SpiB was shown to be critical for the generation of late memory B cells but not early memory B cells or GC B cells, suggesting its role in maintaining humoral memory [1]. In colorectal cancer cells, overexpression of SpiB inhibited cell proliferation, migration, invasion, and angiogenesis, and induced cell-cycle arrest and apoptosis. SpiB also sensitized colorectal cancer cells to oxaliplatin and 5-FU by activating the NF-κB and JNK signaling pathways through MAP4K1 [4]. In ovarian cancer cells, SPIB knockdown inhibited cell progression by down-regulating PD-L1 and inactivating the JAK/STAT pathway [3].

In conclusion, SpiB is a crucial transcription factor involved in multiple biological processes. Studies using KO/CKO mouse models have revealed its significance in B-cell-related functions, as well as in cancer-related processes such as tumor growth, metastasis, and drug resistance. Understanding the role of SpiB may provide new molecular markers and therapeutic targets for diseases like colorectal and ovarian cancers.