PSPC1, known as Paraspeckle component 1, is involved in multiple biological processes. It plays a role in nucleocytoplasmic shuttling, a process dysregulated in cancers and emerging as a cancer hallmark [1,2]. It also has implications in epigenetic regulation as it interacts with proteins like KDM5C in prostate cancer [3].

In acute myeloid leukemia (AML), PSPC1 is aberrantly overexpressed. Using human AML cells and mouse models, loss of PSPC1 in AML cells induced robust differentiation, suppressed proliferation, and abolished leukemogenesis, showing its critical role in maintaining leukemic characteristics [4]. In hepatocellular carcinoma (HCC), PSPC1 is a 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 exhibited synergistic tumor-suppressive effects in HCC cells and mouse models [1].

In conclusion, PSPC1 has diverse functions in biological processes, especially in the context of cancer. Mouse models, such as those used in AML and HCC studies, have revealed its oncogenic roles, highlighting its potential as a therapeutic target in these disease areas.