| First Author | Katiyar S | Year | 2012 |
| Journal | Cancer Res | Volume | 72 |
| Issue | 4 | Pages | 1023-34 |
| PubMed ID | 22174367 | Mgi Jnum | J:181101 |
| Mgi Id | MGI:5308824 | Doi | 10.1158/0008-5472.CAN-11-3647 |
| Citation | Katiyar S, et al. (2012) Mammary Gland Selective Excision of c-Jun Identifies Its Role in mRNA Splicing. Cancer Res 72(4):1023-34 |
| abstractText | The c-jun gene regulates cellular proliferation and apoptosis via direct regulation of cellular gene expression. Alternative splicing of pre-mRNA increases the diversity of protein functions, and alternate splicing events occur in tumors. Here, by targeting the excision of the endogenous c-jun gene within the mouse mammary epithelium, we have identified its selective role as an inhibitor of RNA splicing. Microarray-based assessment of gene expression, on laser capture microdissected c-jun(-/-) mammary epithelium, showed that endogenous c-jun regulates the expression of approximately 50 genes governing RNA splicing. In addition, genome-wide splicing arrays showed that endogenous c-jun regulated the alternate exon of approximately 147 genes, and 18% of these were either alternatively spliced in human tumors or involved in apoptosis. Endogenous c-jun also was shown to reduce splicing activity, which required the c-jun dimerization domain. Together, our findings suggest that c-jun directly attenuates RNA splicing efficiency, which may be of broad biologic importance as alternative splicing plays an important role in both cancer development and therapy resistance. Cancer Res; 72(4); 1023-34. (c)2011 AACR. |
