Pabpc1, the cytoplasmic poly (A) binding protein 1, is a highly conserved multifunctional RNA-binding protein. It is mainly involved in regulating mRNA translation and stability, acting as a central regulator of cytoplasmic mRNA homing, and participating in numerous physiological and pathological processes by influencing almost every aspect of RNA metabolism [1].

In cancer research, Pabpc1 has been found to be aberrantly expressed in various tumors. For example, in pancreatic ductal adenocarcinoma, USP10 deubiquitinates Pabpc1, which then upregulates CLK2 translation to promote tumor progression [2]. In bladder cancer, the circPTK2/Pabpc1/SETDB1 axis promotes EMT-mediated tumor metastasis and gemcitabine resistance [3]. In esophageal squamous cell carcinoma, Pabpc1-induced stabilization of IFI27 mRNA promotes angiogenesis and malignant progression through exosomal miRNA-21-5p [4]. In pancreatic adenocarcinoma, Pabpc1 promotes cell proliferation and metastasis by regulating COL12A1 expression [5]. However, in gliomas, Pabpc1 is downregulated in higher-malignancy cases and may be a potential predictor of the proneural subtype, with higher expression related to better prognosis [6]. Also, Pabpc1 has been implicated in non-cancerous conditions. It mediates the degradation of C9orf72-FTLD/ALS GGGGCC repeat RNA, potentially alleviating related neurodegenerative diseases [7].

In conclusion, Pabpc1 is crucial for mRNA-related functions. Its dysregulation is involved in multiple disease conditions, especially various cancers, where its abnormal expression impacts tumorigenesis, progression, and metastasis. The study of Pabpc1 through different models helps in understanding the underlying molecular mechanisms of these diseases, providing potential directions for diagnosis, treatment, and biomarker discovery.