Therapeutic Considerations for Ron Receptor Expression in Prostate Cancer.

ABSTRACT: Introduction:The Ron receptor tyrosine kinase was initially discovered as a protein which played a critical role in regulating inflammatory responses. This effect was primarily determined through studies in various macrophage populations. Since its initial discovery, a role has emerged for Ron as a driver of cancer within epithelial cells. After numerous publications have detailed a role for Ron in promoting tumor initiation, growth, and metastasis, Ron has been designated as an emerging therapeutic option in a variety of cancers. Areas Covered:This review discusses the current literature regarding the role of Ron in prostate cancer and places special emphasis on the role of Ron in both epithelial cells and macrophages. Whole body loss of Ron signaling initially exposed a variety of prostate cancer growth mechanisms regulated by Ron. With the knowledge that Ron plays an integral part in regulating the function of epithelial cells and macrophages, studies commenced to discern the cell type specific functions for Ron in prostate cancer. A novel role for Ron in promoting Castration Resistant Prostate Cancer has recently been uncovered, and the results of these studies are summarized herein. Furthermore, this review gives a summary of several currently available compounds which show promise at targeting Ron in both epithelial and macrophage populations. Outlook:Sufficient evidence has been provided for the initiation of clinical trials focused on targeting Ron in both macrophage and epithelial compartments for the treatment of prostate cancer. A number of therapeutic avenues for targeting Ron in prostate cancer are currently available; however, special consideration will need to take place knowing that Ron signaling impacts multiple cell types. Further understanding of the cell type specific functions of Ron in prostate cancer will help inform and shape future clinical research and therapeutic strategies.

SUBMITTER: Brown NE 

PROVIDER: S-EPMC6377156 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature