RBM14 enhances transcriptional activity of p23 regulating CXCL1 expression to induce EMT in lung cancer

Abstract

Abstract Metastasis serves as a malignant indicator and biological characteristic of pulmonary carcinoma. Epithelial-mesenchymal transition (EMT) plays a pivotal role in facilitating tumor invasion and metastasis, and enhances the aggressiveness of tumor cells. Prostaglandin E synthase 3 (PTGES3) functions as an HSP90 co-chaperone. Our previous study revealed its HSP90-independent role as a transcription factor involved in cancer-related inflammation. Our present study aims to investigate the impact and mechanism of p23 on lung cancer metastasis. By utilizing cell models in vitro and mouse tail vein metastasis modelsin vivo, our results provide solid evidences that p23 plays a crucial role in promoting lung cancer metastasis through regulating the downstream CXCL1 expression, which is not achieved independently, but rather through formatting a complex with RBM14, thereby facilitating the occurrence and progression of EMT in lung cancer. Therefore, our study demonstrates the potential therapeutic application of the RBM14-p23-CXCL1-EMT axis in targeting lung cancer metastasis.