EZH2 promotes E2F-driven SCLC tumorigenesis through modulation of apoptosis and cell-cycle regulation.

ABSTRACT:

Introduction

Although enhancer of zeste homolog 2 (EZH2) has been associated with both non-small cell and small-cell lung cancers (SCLCs), current observations suggest different mechanisms of EZH2 activation and overexpression in these lung cancer types. Globally, SCLC kills 200,000 people yearly. New clinical approaches for SCLC treatment are required to improve the poor survival rate. Given the therapeutic potential of EZH2 as a target, we sought to delineate the downstream consequences of EZH2 disruption to identify the cellular mechanisms by which EZH2 promotes tumorigenesis in SCLC.

Methods

We generated cells with stable expression of short hairpin RNA targeting EZH2 and corresponding controls (pLKO.1) and determined the consequences of EZH2 knockdown on the cell cycle

SUBMITTER: Hubaux R 

PROVIDER: S-EPMC3713495 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature