Prrx2, the paired-related homeobox transcription factor, is involved in multiple biological processes. It has been associated with pathways such as the Wnt/β -catenin signaling pathway, and is crucial in processes like osteogenic differentiation, cell proliferation, apoptosis, and ferroptosis [2,4,5,6]. It also plays a role in various disease-related mechanisms, making it an important gene for understanding disease pathogenesis [1-9].

In cancer research, silencing Prrx2 in breast cancer cells inhibited their proliferation both in vitro and in nude mouse xenograft models, and it was found to down-regulate the Wnt/β -catenin signaling pathway by suppressing β -catenin expression in the nucleus [6]. In colon cancer, inhibition of Prrx2 decreased the invasive and migrating abilities of cells, hindered epithelial-mesenchymal transition (EMT), and suppressed liver metastasis via inactivation of the Wnt/β -catenin pathway [5]. In glioblastoma, circLRFN5 binds to Prrx2 protein and promotes its degradation, affecting the PRRX2-mediated up-regulation of GCH1, a ferroptosis suppressor [1]. In prostate cancer, activation of Prrx2 promoted enzalutamide resistance, and cells expressing Prrx2 showed alterations in the CDK4/6/Rb/E2F and BCL2 pathways [3]. In lung adenocarcinoma, Prrx2 was highly expressed, acting as a positive regulator of cell proliferation and a negative regulator of apoptosis, and it could bind with the PSMD1 promoter to affect the cells' malignant phenotype [4].

In conclusion, Prrx2 is a key regulator in multiple biological processes and is closely associated with various diseases, especially different types of cancers. The gene knockout or knockdown studies in cell lines and animal models have significantly contributed to understanding its role in cancer-related biological processes such as cell proliferation, metastasis, and ferroptosis, providing potential therapeutic targets for these diseases.