Convergence of oncogenic and hormone receptor pathways promotes pro-metastatic phenotypes.

ABSTRACT: Cyclin D1b is a splice variant of the cell cycle regulator Cyclin D1 and is known to harbor divergent and highly oncogenic functions in human disease. While Cyclin D1b is induced during disease progression in many cancer types, the mechanisms underlying Cyclin D1b function remain poorly understood. Herein, models of human disease were utilized to resolve the downstream pathways requisite for the pro-tumorigenic functions of Cyclin D1b. Specifically, it was shown that Cyclin D1b modulates the expression of a large transcriptional network that cooperates with AR signaling to enhance tumor cell growth and invasive potential. Notably, Cyclin D1b promoted AR-dependent activation of genes associated with metastatic phenotypes. Further exploration determined that transcriptional induction of SN

ORGANISM(S): Homo sapiens

SUBMITTER: Adam Ertel 

PROVIDER: E-GEOD-40794 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress