Abstract 245: An oncogenic role for CCAAT/enhancer binding protein beta in non-small cell lung cancer

Abstract

Abstract The transcription factor CCAAT/enhancer binding protein (C/EBP) beta is known to be a mediator of cellular transformation and tumorigenesis in human colon, breast and ovary cancer. In this study, we focused on C/EBPbeta and its potential role in non-small cell lung cancer (NSCLC). Immunohistochemical staining of 60 human NSCLC samples (adeno- (31), squamous cell - (25), small cell - (1), large cell - (2), and adeno-squamous cell (1) carcinoma) showed that more than 50% of the tumor samples were significantly positive for nuclear staining of C/EBPbeta compared to healthy airway epithelial cells. Retrovirus-delivered siRNA knock-down of C/EBPbeta expression in human NSCLC cell lines A549, H520, and H460 markedly reduced clonogenic growth, which was accompanied by a significant reduction in cyclooxygenase(COX)-2 expression, increase in G0/G1 cells, and PARP cleavage activity. In contrast, using NSCLC cell line Calu-3 with a moderate intrinsic level of C/EBPbeta, forced expression of this transcription factor even increased clonogenic growth and cell proliferation. Whereas recent studies suggested that family member C/EBPalpha has growth-inhibitory properties in airway epithelial cells, our present data indicate an oncogenic role of C/EBPbeta in NSCLC and may represent a new target for cancer co-therapy to increase response to existing chemotherapeutic regimens. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 245.