auThOr’s VIew IL-30 as a New Player in the Immunobiology of Prostate Cancer

As in other types of cancer, the onset and development of prostate cancer depend not only on genetic and epigenetic alterations, but also on multiple signals from the tumor microenvironment. These 2 aberrations may condition each other and synergize in favoring tumor progression.1 In an attempt to decipher microenvironmental messages released within prostate cancer lesions, we ran into the endogenous expression of a newly discovered cytokine, interleukin-30 (IL-30). Originally identified as p28, i.e., a novel polypeptide related to interleukin-12A (IL12A, best known as IL-12p35),2 IL-30 can bind Epstein–Barr virus induced 3 (EBI3) to form IL-27, which has been shown to mediate antineoplastic effects in several tumor models, but also acts as a self-standing cytokine endowed with its own functional properties.3,4 IL-30 may thus be implicated in quite different molecular pathways depending on contextual parameters. As a matter of fact, IL-30 has been ascribed with a tumor-promoting potential as an independent cytokine, at least in the prostate cancer system.5 We have recently shown that the endogenous expression of IL-30 in the prostate and regional lymph node tissue from prostate cancer patients subjected to radical prostatectomy is associated with poorly differentiated, high-grade and metastatic stage of disease.5 Once again, an immunomodulatory molecule, whose functions are for the most part hitherto unknown, has gained a crucial part in the complex scenario of prostate cancer microenvironment. Therein, IL-30 is mostly produced by immune cells of myeloid origin and malignant cells themselves