Abstract A12: A retinoblastoma protein phosphorylation code associated with cell adhesion and invasiveness

Lung cancer remains the leading cause of cancer deaths among men and women worldwide. Its five-year survival rate (17.8%) is by far the lowest among the most common cancers such as colon (65.4%), breast (90.5%), and prostate (99.6%). Early detection and screening still remain challenging, and despite the many recent breakthroughs in lung cancer treatment, improvement in the long-term survival of lung cancer patients is still limited. The inactivation of the retinoblastoma tumor suppressor (Rb) is a major driving force behind tumorigenesis in most cancer types, including lung cancer. Rb is a phosphoprotein traditionally known as a cell cycle repressor. While Rb inactivation in small cell lung carcinomas, osteosarcomas and retinoblastomas occurs by mutational inactivation of the RB1 gene, most other human cancers show Rb inactivation by hyperphosphorylation. The effect of Rb hyperphosphorylation in cell cycle control has been characterized and shown to consist in the abrogation of Rb’s capacity to bind and repress the EF2 transcription factors responsible for triggering S-phase related gene expression. However, our data show that Rb phosphorylation can have novel consequences beyond cell cycle control, and that certain phosphorylations in Rb can impair the cell’s capacity to engage in cell-to-cell interactions. In order to search for phosphorylation patterns that may be associated with cell adhesion defects, we conducted a mass spectroscopy analysis on a panel of E-...
Source: Molecular Cancer Research - Category: Cancer & Oncology Authors: Tags: EMT and Plasticity: Poster Presentations - Proffered Abstracts Source Type: research