PSPC1, also known as Paraspeckle component 1, is involved in multiple biological processes. It plays a role in nucleocytoplasmic shuttling, which is dysregulated in cancers and is emerging as a cancer hallmark. It also participates in pathways related to tumor progression, stem cell bivalency regulation, and cell adhesion and motility. Understanding PSPC1 through genetic models is crucial for uncovering its functions in health and disease [1,2,5,6].

In hepatocellular carcinoma (HCC) progression, PSPC1 is the contextual determinant of the TGF-β prometastatic switch and PTK6/β -catenin reciprocal oncogenic nucleocytoplasmic shuttling. The PSPC1 C -terminal 131 polypeptide (PSPC1 -CT131) targeting PSPC1 and PTK6 has tumor -suppressive effects in HCC cells and mouse models [1]. In prostate cancer, PSPC1 is up -regulated in primary and metastatic tumors, and its elevated expression correlates with poor prognosis [3]. In acute myeloid leukemia (AML), PSPC1 is aberrantly overexpressed. PSPC1 loss in human AML cells and mouse models induces differentiation, suppresses proliferation, and abolishes leukemogenesis [4].

In conclusion, PSPC1 is a significant factor in multiple disease -related biological processes, especially in cancer progression. Studies using mouse models have revealed its oncogenic roles in HCC, prostate cancer, and AML, highlighting its potential as a therapeutic target in these diseases.