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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RB Dysfunction in Pancreatic Cancer Enables TGF-beta to Promote Proliferation

ABSTRACT: Pooled KRC (LSL-KrasG12D; Rb1L/L; Pdx1-Cre: oncogenic Kras and deleted Rb1 in the pancreas) cells derived from 2 month old mice were compared to pooled KC (LSL-KrasG12D; Pdx1-Cre: oncogenic Kras in the pancreas) cells derived from 8 month old mice.

ORGANISM(S): Mus musculus

SUBMITTER: Kelly Craven

PROVIDER: E-MEXP-3988 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Pancreatic cancer-associated retinoblastoma 1 dysfunction enables TGF-β to promote proliferation.

Gore A Jesse AJ Deitz Samantha L SL Palam Lakshmi Reddy LR Craven Kelly E KE Korc Murray M

The Journal of clinical investigation 20131216 1

Pancreatic ductal adenocarcinoma (PDAC) is often associated with overexpression of TGF-β. Given its tumor suppressor functions, it is unclear whether TGF-β is a valid therapeutic target for PDAC. Here, we found that proliferating pancreatic cancer cells (PCCs) from human PDAC patients and multiple murine models of PDAC (mPDAC) often exhibit abundant levels of phosphorylated retinoblastoma 1 (RB) and Smad2. TGF-β1 treatment enhanced proliferation of PCCs isolated from KrasG12D-driven mPDAC that l ...[more]

PMID: 24334458

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