Transcriptional effects of CTGF inhibition and gemcitabine in the KPC mouse model of pancreatic ductal adenocarcinoma
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ABSTRACT: Pancreatic ductal adenocarcinoma (PDA) is characterized by abundant desmoplasia and poor tissue perfusion. These features are proposed to limit access of therapies to neoplastic cells and blunt treatment efficacy. Indeed, several agents that target the PDA microenvironment promote chemotherapy delivery and improve anti-neoplastic responses in murine models of PDA. Here, we employed the FG-3019 monoclonal antibody directed against the pleiotropic matricellular signaling molecule connective tissue growth factor (CTGF/CCN2). FG-3019 treatment increased PDA cell killing and led to a dramatic tumor response without altering gemcitabine delivery. Microarray expression profiling revealed the down-regulation by FG-3019 of several anti-apoptotic transcripts, including the master regulator Xiap, dow
ORGANISM(S): Mus musculus
SUBMITTER: Mark Sternlicht
PROVIDER: E-GEOD-46203 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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