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Accepted (AM)Open Access (License Unspecified), Open
Journal article
Retinoblastoma protein potentiates the innate immune response in hepatocytes: significance to hepatocellular carcinoma
Hepatology (Baltimore, Md.), v 60(4), pp 1231-1240
28 Aug 2014
PMID: 24824777
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Cancers mediated by viral etiology must exhibit deregulated cellular proliferation and evade immune recognition. The role of the retinoblastoma tumor suppressor (RB) pathway, which is lost at relatively high frequency in HCC, has recently been expanded to include the regulation of innate immune responsiveness. In this study, we investigated the coordinate impact of RB-loss on cell cycle control and immune function in the liver. We found that RB depletion in hepatoma cells resulted in a compromised immunological response to multiple stimuli and reduced the potential of these cells to recruit myeloid cells. Viral-mediated liver-specific RB deletion
in vivo
led to the induction of genes associated with proliferation and cell cycle entry as well as the significant attenuation of genes associated with immune function, as evidenced by decreases in cytokine and chemokine expression, leukocyte recruitment and hepatic inflammation. To determine if these changes in gene expression were instructive in human disease, we compared our liver-specific RB-loss gene signature to existing profiles of HCC and found that this signature was associated with disease progression and confers a worse prognosis.
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Details
- Title
- Retinoblastoma protein potentiates the innate immune response in hepatocytes: significance to hepatocellular carcinoma
- Creators
- Jack Hutcheson - The University of Texas Southwestern Medical CenterRyan J. Bourgo - Kimmel Cancer CenterUthra Balaji - The University of Texas Southwestern Medical CenterAdam Ertel - Sidney Kimmel Cancer CenterAgnieszka K. Witkiewicz - South Australia PathologyErik S. Knudsen - The University of Texas Southwestern Medical Center
- Publication Details
- Hepatology (Baltimore, Md.), v 60(4), pp 1231-1240
- Publisher
- Wiley
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- School of Biomedical Engineering, Science, and Health Systems
- Web of Science ID
- WOS:000342662100016
- Scopus ID
- 2-s2.0-84927768777
- Other Identifier
- 991019176804504721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Gastroenterology & Hepatology