Cpsf4, short for Cleavage and polyadenylation specificity factor 4, is a crucial component of the pre-mRNA 3' end processing complex, which is involved in RNA alternative splicing (AS), an important stage in controlling gene expression [4].

In multiple cancer types, Cpsf4 has been shown to act as an oncogene. In lung cancer, it promotes the tumor-initiating phenotype and chemoresistance by enhancing VEGF/NRP2/TAZ signaling [1]. In hepatocellular carcinoma (HCC), Cpsf4 reduces circRNA levels, disrupts miRNA-mediated gene silencing, and promotes cell proliferation [2]. In triple-negative breast cancer, it promotes metastasis by upregulating MDM4 [3], and also regulates alternative splicing of HMG20B to facilitate cancer progression [6]. In oral squamous cell carcinoma, Cpsf4 promotes cell proliferation and invasion via the PI3K-AKT signaling pathway [5]. In prostate cancer, high Cpsf4 expression is associated with enhanced cell migration and cell cycle dysregulation [8]. In bladder cancer, knockdown of Cpsf4 inhibits cell growth by upregulating NRF1 [9]. In breast cancer, miR-4458 can inhibit cell growth, migration, and invasiveness by targeting Cpsf4 [10]. In lung adenocarcinomas, Cpsf4 activates telomerase reverse transcriptase and is associated with poor prognosis [7].

In conclusion, Cpsf4 is significantly involved in the regulation of multiple biological processes related to cancer development, such as cell proliferation, invasion, metastasis, and chemoresistance. Studies, including those using knockdown models (functionally similar to gene-knockout in revealing gene function), have shown its oncogenic role across various cancer types, highlighting its potential as a prognostic marker and therapeutic target in cancer research.