Paip1, short for Poly(A)-binding protein interacting protein 1, is a translational initiation regulatory factor. It binds to PABP and is involved in the regulation of translation initiation, which is crucial for protein synthesis, a fundamental biological process. It has been associated with several biological pathways and is of great importance in normal and disease-related biological contexts [2].

In multiple cancers, Paip1 has shown oncogenic properties. In hepatocellular carcinoma (HCC), its knockdown inhibits cell proliferation, colony formation, and tumorigenesis, while inducing apoptosis and altering cell cycle distribution by increasing the G2/M cell percentage. Bioinformatics and immunoblotting analysis reveal it dysregulates cyclin D pathway-related proteins [1]. In pancreatic cancer, Paip1 silencing inhibits cell proliferation, metastasis, and angiogenesis, with over-expression having opposite effects [2]. In cervical cancer, knockdown of Paip1 inhibits cell growth, induces apoptosis and cell cycle arrest, and the in vivo tumor model confirms its pro-tumor role [3]. In oral squamous cell carcinoma, PAIP1 knockdown attenuates colony-forming ability and aggressiveness, decreasing MMP9 activity and SRC phosphorylation [4]. In lung adenocarcinoma, Paip1 depletion attenuates cell proliferation and migration, and it regulates the AKT/GSK-3β oncogenic signaling pathways [5].

In conclusion, Paip1 is a key translational initiation regulatory factor. Its over-expression in various cancers, as shown through loss-of-function experiments including knockdowns in different cell lines and in vivo murine models, promotes tumor progression. These findings emphasize its significance as a potential target for cancer treatment and as a prognostic marker in multiple cancer types.