Kpnb1, also known as karyopherin subunit beta-1, is a member of the karyopherin β family. It plays a crucial role in mediating the transportation of proteins from the cytoplasm to the nucleus, which is essential for maintaining cellular homeostasis. This process is involved in various biological pathways, such as those related to cell proliferation, differentiation, and circadian rhythm regulation [1,4,7].

In cancer research, down-regulation of Kpnb1 level and inhibition of its activity prevent the entry of cancer-related transcription factors into the nucleus, suppressing cancer cell proliferation and metastasis. For example, in glioblastoma, knockdown of Kpnb1 inhibited tumor progression both in vitro and in vivo, as Kpnb1 regulated GBM progression through the YBX1-NLGN3 axis [2]. In non-small cell lung cancer, Kpnb1-mediated nuclear translocation of PD-L1 promoted cell proliferation via the Gas6/MerTK signaling pathway [3]. In acute myeloid leukemia, knockdown of Kpnb1 led to growth inhibition and apoptosis in AML cells, and its pharmacological inhibition enhanced the sensitivity of AML cells to venetoclax [5]. In gastric cancer, inhibition of Kpnb1 with genkwadaphnin suppressed cancer progression through the Nur77-mediated signaling pathway [6].

In conclusion, Kpnb1 is essential for nucleocytoplasmic shuttling, influencing various biological processes. Studies using loss-of-function models, including knockdown experiments in cancer cells, have revealed its significant role in cancer development and progression, highlighting its potential as a therapeutic target in cancer treatment.