Anti-CTBP1 (full length) polyclonal antibody

Recent advances in genomic approaches for exploring the transcriptome have led to the identification of thousands of novel non-coding RNA (ncRNA) transcripts (Djebali et al, 2012). While some of these ncRNAs have been implicated in the development and progression of cancer and other human diseases, their underlying mechanisms of action remain largely unknown (Esteller, 2011). Takayama et al (2013) now report the identification of CTBP1-AS, a novel androgen-regulated long ncRNA that promotes prostate cancer growth through sense-antisense repression of the transcriptional co-regulator CTBP1, as well as through the global epigenetic regulation of tumour suppressor genes.

Carboxyl-terminal binding protein 1 (CtBP1) is a transcriptional co-repressor with oncogenic potential. Immunohistochemistry staining using human breast cancer tissue arrays revealed that 92% of invasive ductal breast cancer cases have CtBP1-positive staining compared to 4% CtBP1-positive in normal breast tissue. To explore the functional impact of CtBP1 in breast cancer, we examined CtBP1's transcriptional regulation of known tumor suppressors, breast cancer susceptibility gene 1 (Brca1), and E-cadherin. We found CtBP1 was recruited to the promoter regions of Brca1 and E-cadherin genes in breast cancer cells. Concomitantly, Brca1 loss was detected in 57% and E-cadherin loss was detected in 76% of human invasive ductal breast cancers, and correlated with CtBP1 nuclear staining in these lesions. Importantly, siRNA knock down of CtBP1 restored Brca1 and E-cadherin expression in breast cancer cell lines, implying CtBP1 down-regulates Brca1 and E-cadherin genes in human breast cancer. This study provides evidence that although genetic loss of Brca1 and E-cadherin are infrequent in breast cancer, they are down-regulated at the transcriptional level by CtBP1 expression. Thus, CtBP1 activation could be a potential biomarker for breast cancer development. (C) 2011 Wiley Periodicals, Inc.