Heme oxygenase 1 governs the cytoskeleton at filopodia: pulling the brakes on the migratory capacity of prostate tumoral cells

Abstract

This paper refers to Paez et al.1 Prostate cancer (PCa) is the second leading cause of cancer death in men in the United States.2 Incidence increases with patient age and represents the most important risk factor. Localized PCa can be cured in most cases, but when the disease escapes the confines of the gland, the prospects for cure decrease drastically. Androgen ablation is the most effective way of halting PCa progression, but given sufficient time, growth of the cancer resumes in most cases and the disease becomes castration resistant (castration-resistant PCa (CRPC)).3 No therapy is curative for patients with CRPC, thus emerging a critical need to identify new therapy targets. Advanced PCa has been associated to the loss of cell adhesion molecules at adherens junctions.4 The delicate equilibrium between the cell pushing and pulling forces drive leading edge dynamics and cell migration. Interdigitating filopodia are vital for the proper alignment and establishment of the initial cell?cell adhesions, known as adhesion zippering, an event that contributes significantly to reduce the metastatic phenotype of tumor cells.