Document Type
Article
Publication Date
6-1-2017
Abstract
Pancreatic ductal adenocarcinoma (PDA) is the third leading cause of cancer-related deaths in the United States, whereas colorectal cancer is the third most common cancer. The RNA-binding protein HuR (ELAVL1) supports a pro-oncogenic network in gastrointestinal (GI) cancer cells through enhanced HuR expression. Using a publically available database, HuR expression levels were determined to be increased in primary PDA and colorectal cancer tumor cohorts as compared with normal pancreas and colon tissues, respectively. CRISPR/Cas9 technology was successfully used to delete the HuR gene in both PDA (MIA PaCa-2 and Hs 766T) and colorectal cancer (HCT116) cell lines. HuR deficiency has a mild phenotype,
Recommended Citation
Lal, Shruti; Cheung, Edwin C,; Zarei, Mahsa; Preet, Ranjan; Chand, Saswati N.; Mambelli-Lisboa, Nicole C.; Romeo, Carmella; Stout, Matthew C.; Londin, Eric; Goetz, Austin; Lowder, Cinthya Y.; Nevler, Avinoam; Yeo, Charles; Campbell, Paul M.; Winter, Jordan M.; Dixon, Dan A.; and Brody, Jonathan, "CRISPR Knockout of the HuR Gene Causes a Xenograft Lethal Phenotype." (2017). Department of Surgery Faculty Papers. Paper 159.
https://jdc.jefferson.edu/surgeryfp/159
PubMed ID
28242812
Language
English
Comments
This article has been peer reviewed. It is the authors' final version prior to publication in Molecular Cancer Research, Volume 15, Issue 6, June 2017, Pages 696-707.
The published version is available at https://doi.org/10.1158/1541-7786.MCR-16-0361. Copyright © American Association for Cancer Research