Posttranscriptional Regulation of
Publication/Presentation Date
9-15-2017
Abstract
The majority of pancreatic ductal adenocarcinomas (PDAC) rely on the mRNA stability factor HuR (ELAV-L1) to drive cancer growth and progression. Here, we show that CRISPR-Cas9-mediated silencing of the HuR locus increases the relative sensitivity of PDAC cells to PARP inhibitors (PARPi). PDAC cells treated with PARPi stimulated translocation of HuR from the nucleus to the cytoplasm, specifically promoting stabilization of a new target, poly (ADP-ribose) glycohydrolase (
Volume
77
Issue
18
First Page
5011
Last Page
5025
ISSN
1538-7445
Published In/Presented At
Chand, S. N., Zarei, M., Schiewer, M. J., Kamath, A. R., Romeo, C., Lal, S., Cozzitorto, J. A., Nevler, A., Scolaro, L., Londin, E., Jiang, W., Meisner-Kober, N., Pishvaian, M. J., Knudsen, K. E., Yeo, C. J., Pascal, J. M., Winter, J. M., & Brody, J. R. (2017). Posttranscriptional Regulation of PARG mRNA by HuR Facilitates DNA Repair and Resistance to PARP Inhibitors. Cancer research, 77(18), 5011–5025. https://doi.org/10.1158/0008-5472.CAN-16-2704
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
28687616
Department(s)
Administration and Leadership
Document Type
Article