P. Y. WuY. C. LinY. L. HuangW. M. ChenC. C. ChenH. Lee2019-04-152019-04-1520182072-6694https://scholars.lib.ntu.edu.tw/handle/123456789/405427https://www.scopus.com/inward/record.uri?eid=2-s2.0-85056088139&doi=10.3390%2fcancers10110413&partnerID=40&md5=e5f188212d8802c34b0933186f95b3fcProstate cancer (PCa) is the most common noncutaneous cancer in men worldwide. One of its major treatments is androgen deprivation therapy, but PCa frequently relapses as aggressive castration resistant local tumors and distal metastases. Hence, the development of novel agents or treatment modalities for advanced PCa is crucial. Many tumors, including PCa, first metastasize to regional lymph nodes via lymphatic vessels. Recent findings demonstrate that the bioactive lipid lysophosphatidic acid (LPA) promotes PCa progression by regulating vascular endothelial growth factor-C (VEGF-C), a critical mediator of tumor lymphangiogenesis and lymphatic metastasis. Many of the underlying molecular mechanisms of the LPA–VEGF-C axis have been described, revealing potential biomarkers and therapeutic targets that may aid in the diagnosis and treatment of advanced PCa. Herein, we review the literature that illustrates a functional role for LPA signaling in PCa progression. These discoveries may be especially applicable to anti-lymphangiogenic strategies for the prevention and therapy of metastatic PCa. ? 2018 by the authors. Licensee MDPI, Basel, Switzerland.LPA; LPA receptor; Lymphangiogenesis; Prostate cancer; VEGF-C[SDGs]SDG3antineoplastic agent; lysophosphatidic acid; lysophosphatidic acid receptor; lysophosphatidic acid receptor antagonist; mitogen activated protein kinase; protein serine threonine kinase inhibitor; protein tyrosine kinase inhibitor; unclassified drug; vasculotropin C; cancer growth; cancer prevention; carcinogenesis; disease association; human; hyperglycemia; lymph node metastasis; lymphangiogenesis; molecular pathology; nonhuman; prostate cancer; protein expression; protein function; protein lipid interaction; Review; signal transduction; tumor invasion; tumor vascularizationreview10.3390/cancers101104132-s2.0-85056088139